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& 




TREATMENT OF CASUALTIES 


FROM 


CHEMICAL WARFARE A6ENTS 


NAVMED 220 



A MANUAL 

FOR THE INFORMATION AND GUIDANCE 
OF MEDICAL OFFICERS 
UNITED STATES NAVY 


20 JULY 1944 







RESTRICTE%<^‘ 

<$A# X 


v\> ^\ V «Wr \ 

AA*' 


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<y 


MANUAL ON 


TREATMENT OF CASUALTIES 

FROM 

CHEMICAL WARFARE AGENTS 


NAVMED 220 



THE BUREAU OF MEDICINE AND SURGERY. 

A 

NAVY DEPARTMENT 
1944 


United States Government Printing Office 
Washington: 1944 













\ 


PREFACE 

This Manual on the Treatment of Casualties from Chemical Warfare Agents 
is published for the information and guidance of medical officers. 

Its purpose is to make available in concise form the most recent and generally 
accepted data concerning self-aid, first-aid, and definitive treatment of casualties 
from Chemical Warfare Agents. Certain additional topics with respect to gas 
defense falling under the cognizance of the medical officer, have also been 
included. 

This material is largely based upon the latest revision of Technical Manual 
TM 8-285, Treatment of Casualties from Chemical Agents, War Department 
Representatives of the Medical Corps of the Navy and of the Committee on 
the Treatment of Gas Casualties of the National Research Council collaborated 
with representatives of the Medical Division of the Chemical Warfare Service, 
War Department in the preparation of this revision. Acknowledgment is 
made herewith to the Surgeon General, United States Army, for authority to 
duplicate certain chapters. 


Ross T Mclntire 

Surgeon General, United States Navy 


II 


o 

ul 


TABLE OF CONTENTS 


p3 

J 

Section I. General ... 

Section II. Lung Irritants (Choking Gases)... 

Phosgene (CG) and Diphosgene (DP) . 

Chlorpicrin (PS) . 

Chlorine (CL) . 

Nitric (Nitrous) Fumes . 


Page 

1 

3 

o 

D 

6 

6 

6 


Section III. Vesicants (Blister Gases) . 9 

Mustard (H) . 10 

Nitrogen Mustards (HN) . 20 

Lewisite (L) . 25 

Ethyldichlorarsine (ED) . 29 

Phenyldichlorarsine (PD) . 30 

Mixed Blister Gases . 30 

Section IV. Lacrimators (Tear Gases) . 33 

Chloracetophenone (CN) . 33 

Chloracetophenone Solution (CNS) . 33 

Chloracetophenone Training Solution (CNB) . 33 

. Brombenzyl Cyanide (BBC) . 33 

Section V. Vomiting Gases (Nose gases, irritant smokes, sternu- 

» tators) . 35 

Diphenylaminechlorarsine (DM) (Adamsite) . 35 

Diphenylchlorarsine (DA) . 36 

Diphenylcyanarsine (DC) . 36 


Section VI. Screening Smokes . 37 

White Phosphorus (WP) . 37 

Titanium Tetrachloride (FM) . 37 

Sulfur Trioxide-Chlorsulfonic acid solution (FS) 

HC Mixture (HC) . 38 


III 



























Page 


Section VII. Incendiary Agents . 39 

Thermite (TH) . 39 

Magnesium (TH) . 39 

White Phosphorus (WP) . 39 

Oil Incendiaries . 40 

Section VIII. Systemic Poisons (Blood and Nerve Poisons) . 41 

Hydrocyanic Acid (AC) . 41 

Cyanogen Chloride (CC) . 42 

Arsine (SA) . 43 

Section IX. Incidental Gases . 45 

Carbon Monoxide . 45 

Ammonia . 46 

Hydrogen Sulfide (H 2 S) . 46 

Section X. The Treatment of Thermal Burns . 49 

Section XI. Care of Contaminated Clothing and Equipment 

at Medical Installations . 53 

Section XII. Disinfection of Gas Masks . 55 

Section XIII. Chemical Agent Contamination of Food . 57 

Section XIV. The Detection of Water Contaminated with 

Chemical Warfare Agents . 61 

Section XV. The Management and Transport of Chemical 

Warfare Casualties in Naval and Marine 
Forces . 69 

Section XVI. Naval Medical Supply Depot Items for the 

Treatment of Chemical Warfare Casualties 73 

Section XVII. Syllabus of Instruction and Training in Chemi¬ 
cal Warfare Defense for all Medical Per¬ 
sonnel . 77 

Index. 79 

Chemical Warfare Reference Chart . 


IV 
























SECTION 1 
GENERAL 


1. INTRODUCTION 

A. Chemical warfare agents are used to produce casualties, to make areas 
both ashore and afloat impassable or untenable, to render food, water and 
material unusable, to provide concealment and to start fires. 

B. The scope of chemical warfare is broad. It aims at groups rather than 
individuals. Gas may penetrate turrets, compartments, emplacements, dug- 
outs and trenches. Projected from the airplane, chemical agents may produce 
casualties and contamination in topside battle stations, or within ships even 
though far out to sea, as well as on shore stations, beaches or far back into 
rear areas. 

C. In contemplating casualties due to gas attack cognizance must be given 
to specific problems pertaining to naval operations in contrast to shore opera¬ 
tions. Especially should it be stressed that contaminated areas on land may 
be avoided, whereas at sea, once a ship is contaminated, the personnel must 
not only continue to fight in the contaminated area, but will be forced to eat, 
sleep, rest and live in it until decontaminated. 

D. The medical officer must be familiar with the tactics of chemical attack 
and the methods of defense to lessen or neutralize its effect. He must realize 
that the most effective gas defense for personnel demands fearless action, the 
best possible use of protective equipment and, when exposed, prompt self-aid. 

E. The medical officer afloat must be acquainted with the damage control 
organization of the ship. He must formulate his plans accordingly and in con¬ 
formity with the necessary compromise between the function of the ship as a 
combat unit and the effective handling of casualties when they occur. Stations 
for the decontamination of wounded gas casualties must be so placed as to be 
available quickly without contaminating otherwise clean passageways and com¬ 
partments. 

F. The medical officer attached to shore activities must appreciate the prob¬ 
lems specific to such activities. He must devise plans for the care of gassed 
cases with additional injury whether they be in forward areas or on shore sta¬ 
tions within range of gas attack. Undue delay in decontamination must be 
avoided and gas-contaminated personnel must be denied admission to medical 
installations not specifically designated to handle such cases. 

G. The purpose of this manual is to acquaint medical personnel with the 
treatment of casualties produced by chemical agents. 


1 


2. CLASSIFICATION OF AGENTS 


Chemical warfare agents are classified according to their physiological action, 
persistency, and tactical use. 

A. Classification by Physiological Action .—(1) Lung irritants (choking 
gases) primarily irritate and damage the respiratory tract. Example: Phos¬ 
gene. 

(2) Vesicants (blister gases) injure the eyes, produce reddening and blister¬ 
ing of the skin, and when inhaled damage the respiratory tract. Example: 
mustard. 

(3) Lacrimators (tear gases) act primarily on the eyes, causing tears and 
intense, though temporary, pain. Example: chloracetophenone. 

(4) Irritant smokes or sternutators (vomiting gases) irritate the nose, 
throat and eyes. They may produce temporary prostration. Example: diphenyl- 
aminechlorarsine (adamsite). 

(5) Systemic poisons (blood and nerve poisons) stop essential physiological 
processes. Example: hydrocyanic acid. 

B. Classification by Persistency. —The ability of an agent to maintain an 
effective concentration under field conditions is called its persistency. 

(1) Persistent agents maintain effective concentrations longer than 10 
minutes, and then may last for days or weeks. They are used to neutralize or 
force evacuation of certain areas. Example: mustard. 

(2) Non persistent agents maintain effective concentrations less than 10 
minutes. They do not render ground untenable after the cloud has passed. 
Example: phosgene. 

C. Classification by Tactical Use. (1) Casualty agents injure personnel. 
Example: mustard and phosgene. 

(2) Harassing agents force the wearing of masks and thus impede opera¬ 
tions. Example: irritant smoke. 

(3) Screening agents produce obscuring smoke to prevent observation. Ex¬ 
ample: white phosphorus. 

(4) Incendiaries ignite materiel and produce burns on personnel. Example: 
thermite. 

3. FUNDAMENTALS OF SELF-AID AND TREATMENT 

A. Prompt Self-Aid is the most important factor in reducing the number of 
gas casualties. It is concerned with the removal and neutralization of the 
chemical agent before serious injury occurs. Unless incapacitated, each man 
will care for himself at the earliest possible moment. 

B. Definitive Treatment is designed to promote healing after injury has oc¬ 
curred and should be differentiated from Self-Aid. This is the function of the 
Medical Department. 


2 


SECTION II 

LUNG IRRITANTS 


4. GENERAL 

A. The primary lung irritants are phosgene, diphosgene, chlorpicrin, chlo¬ 
rine and nitrous fumes. In general, the gases which are the most irritating, such 
as chlorine and chlorpicrin, are most likely to injure the trachea and bronchi. 
Those which are less irritating, such as phosgene and nitrous fumes, produce 
their major effect on the lungs and cause pulmonary edema. In addition to 
the above-designated lung irritants, vesicants and certain systemic poisons also 
damage the respiratory tract. (See sections III and VIII.) 

B. Personnel exposed to a lung-irritant gas need not be withdrawn during 
combat unless signs of pulmonary distress are apparent. The medical officer 
should so advise the responsible commanding officer. 

C. The service mask and collective protector offer adequate protection. On 
detection, hold the breath instantly, apply the mask and exhale as completely 
as possible. Speed is absolutely essential. 


5. PHOSGENE (CG) AND DIPHOSGENE (DP) 

Phosgene and Diphosgene are essentially similar in pathology, symptoms and 
treatment. 

A. Pathology .—Phosgene has no effect on the skin. In the upper respira¬ 
tory tract and the eyes it may produce a mild inflammatory reaction. Its main 
sites of action are the bronchioles and alveoli. Congestion, edema and mild 
cellular infiltration of the bronchiolar or alveolar wall, with alternating patches 
of emphysema, are present soon after exposure. The permeability of the capil¬ 
laries is increased, and plasma-like fluid escapes into the alveoli. This accumu¬ 
lation of fluid reduces the space vital for respiratory exchange, fills many of the 
bronchioles, and produces pulmonary consolidation. Areas of lung not so con¬ 
solidated become emphysematous. As plasma is lost into the lungs, hemocon- 
centration and anoxemia result. Small hemorrhages, due to the anoxia, are 
frequent in the lungs and elsewhere, especially in the central nervous system. 
Death may result finally from oxygen want. If recovery takes place, the fluid 
in the lungs is absorbed or expectorated. Patchy areas of fibrosis represent the 


3 


healed lung lesion. This focal scarring follows the injury by the gas and 
usually is not a result of a bacterial bronchopneumonia. Occasionally, however, 
a bacterial pneumonia may be superimposed. 

B. Symptoms. —Immediately after exposure there is likely to be coughing, 
choking, a feeling of tightness in the chest, and lacrimation. The presence or 
absence of these symptoms is of little value in immediate prognosis as some 
patients with severe cough fail to develop serious lung injury, while others 
with no signs of respiratory tract irritation go on to fatal pulmonary edema. 
There may be slowing of the pulse initially, followed usually by an increase in 
rate. This transient bradycardia is presumptive evidence of phosgene poisoning. 
A period follows during which abnormal chest signs are absent and the patient 
may be symptom-free. This interval commonly lasts 2 to 24 hours, but oc¬ 
casionally is shorter. It is terminated by the signs and symptoms of pulmonary 
edema. These begin with rapid, shallow breathing, painful cough, and 
cyanosis (blue stage). Nausea and vomiting may appear. As the edema 
progresses, discomfort, apprehension and dyspnea increase, and much frothy 
sputum is raised. Rales and rhonchi are audible over the chest. The patient 
may develop a shock-like state with leaden, clammy skin, low blood-pressure 
and a feeble heart (gray stage). 

C. Diagnosis.— Irritation of the nose and throat by phosgene may be mis¬ 
taken for an upper respiratory tract infection. Difficulty in breathing and 
complaint of tightness in the chest may suggest an acute asthmatic attack. The 
pulmonary edema is like that produced by many other war gases and may be 
confused with the edema associated with heart failure. Diagnosis can be 
established with certainty only from a definite history of exposure to phosgene, 
the odor suggesting musty or burned hay, silage or green corn. 

D. Treatment .—(1) Rest.— Pending the appearance of definite symptoms, 
men may continue their duties. When symptoms appear, if there is no res¬ 
piratory distress with moderate exertion, casualties may be evacuated by walk¬ 
ing. Essential equipment may be carried. Unnecessary exertion is to be 
avoided. 

(2) Warmth .—Phosgene casualties should be kept only comfortably warm. 

(3) Oxygen therapy .—Anoxia should be treated with oxygen. The need 
for oxygen is indicated by cough, dyspnea, cyanosis and restlessness. Oxygen 
should be administered in as high a concentration as possible, in any case high 
enough to eliminate cyanosis. Oxygen decreases anoxia and quiets the patients. 
It is best administered by a mask which allows regulation of the proportions 
of oxygen and air. Lower and less well-controlled concentrations of oxygen 
are obtainable in tents and with nasal catheters. Carbon dioxide-oxygen mix¬ 
tures are not indicated in phosgene poisoning. 

(4) Venesection. —-There is at present no definite evidence that venesection 
is beneficial at any time; it is certainly harmful during the shock-like state. 


4 


O) Sedation — 11 oxygen fails to quiet the patient, morphine may he used 
subcutaneously in a dose of ,01 to .015 grams (grains 1/6 to ^). The physi¬ 
cian must weigh the value of its sedative effect against its depression of respira¬ 
tion. Codeine may be more useful than morphine if cough is the prominent 
symptom. Sedative doses of barbiturates are ineffective and larger doses may 
be harmful. 

(6) Chemotherapy .—Sulfonamides should not be given during the latent 
period. Thereafter they should be administered for the prevention of 
pulmonary infection as soon as the edema begins to subside, as evidenced by an 
improvement in the patient’s general condition. Two grams (grains 30) of 
sulfadiazine should be given initially, followed by 1 gram (grains 15) every 
six hours for five to seven days. The urine should be kept alkaline during 
sulfonamide therapy by the administration of 2 grams (grains 30) of sodium 
bicarbonate every 4 hours. Sufficient fluids should be given to maintain a 
daily urinary output of at least 1 liter (about 1 quart). 

(7) Expectorants .—Expectorants should not be used in the treatment of 
pulmonary edema. They may be of value in relieving cough when irritation 
is limited to the upper respiratory tract. 

(8) Other measures .—Atropine does not diminish edema or improve breath¬ 
ing; its acceleratory action on the heart is undesirable. Plasma is of no value 
in the treatment of phosgene poisoning. Infusions pass readily into the lungs 
and increase the edema. Concentrated plasma is even more harmful. Surgery, 
except* emergency measures to save life, is contraindicated in the active stage of 
edema. If anesthesia is required, local infiltration or nerve block is the method 
of choice. Cardiac and respiratory stimulants, such as adrenalin, ephedrine, 
benzedrine, coramine, and metrazol do more harm than good. Alcohol is 
contraindicated. 

E. Convalescent care .—Absolute rest must be continued until the acute 
symptoms have disappeared. As recovery progresses, exercise should be re¬ 
sumed gradually. Sitting in bed should be permitted first, then for brief in¬ 
tervals in a chair. Bathroom privileges should follow and then short periods 
of alternate walking and resting. Later the convalescent should walk increas¬ 
ing distances. 

F. Prognosis. —Prognosis should be guarded because of the insidious nature 
of the poisoning. Most deaths occur within the first 48 hours. The few which 
occur later are due largely to bronchopneumonia. Casualties from phosgene 
which survive more than 48 hours usually recover without sequelae. Rarely 
chronic bronchitis and bronchiectasis result. The incidence of tuberculosis is 
not greater in men with a history of phosgene poisoning than in the general 
population. 


3 


6. CHLORPICRIN (PS) 

A. Pathology. —(1) Chlorpicrin vapor produces conjunctivitis and may, 
after severe exposure, cause corneal ulceration. 

(2) The epithelium of the respiratory tract is injured by chlorpicrin. In the 
trachea and large bronchi the damage may be only slight and temporary, but 
in the small bronchi there is more necrosis of the epithelium than is produced 
by either phosgene or chlorine. In the alveoli chlorpicrin produces less injury 
than phosgene, but more than chlorine. 

(3) The vapor of chlorpicrin irritates the skin, and the liquid can produce 
deep burns. 

B. Symptoms .—Irritation of the eyes is the first symptom noted, as chlor¬ 
picrin is a strong lacrimator. This is frequently followed by pain in the chest, 
cough, nausea and vomiting. Severe exposure causes pulmonary edema, like 
that produced by phosgene, and generalized muscular weakness, with feeble 
heart action. Repeated small exposures increase susceptibility to asthmatic 
attacks from traces of this gas. 

C. Diagnosis .—Diagnosis can be established by a history of exposure, a char¬ 
acteristic fly paper odor on clothing and the symptoms described above. 

D. Treatme77t .—Irritation of the eyes and nose can be relieved by irrigation 
with water, followed by the instillation of butyn ophthalmic ointment or a 
few drops of solution, anesthetic. Inhalation of steam relieves the tracheobron¬ 
chial irritation. Codeine helps to allay the cough. If pulmonary edema 
develops, it is treated like that caused by phosgene. (See par. 5 D, page 4.) 

E. Prognosis .—Most deaths occur in the first 24 hours and if later, are due 
usually to bronchopneumonia. Casualties surviving this period generally re¬ 
cover without sequelae. 


7. CHLORINE (CL) 

A. Chlorine is very irritating to the respiratory tract. It produces damage 
which may result in necrosis of the mucous membrane of the trachea, bronchi 
and lungs. Pulmonary edema occurs, and is similar to that caused by phosgene. 
After exposure, the initial symptoms are burning in the throat, violent cough¬ 
ing, and a feeling of suffocation. Pulmonary edema follows sometimes within 
20 minutes. The history and the intense irritation of the nose and throat are 
aids to early diagnosis. The treatment of chlorine poisoning is the same as 
that outlined for chlorpicrin. (See par. 6 D, page 6.) 

.8. NITRIC (NITROUS) FUMES 

A. Properties .—Nitric fumes consist chiefly of mixtures of the oxides of 
nitrogen. They are orange-yellow to red-brown in color, soluble in water, and 
react with water and oxygen to form nitrous and nitric acids. 


6 


B. Occurrence of poisoning .— The danger of nitrous fume poisoning is great 
if high explosives such as smokeless powder or cordite are burned or detonated 
under conditions of deficient ventilation. This may occur in gun pits and 
armored vehicles, ship magazines and turrets, as well as in mining and tunnel¬ 
ing operations. Nitrogen dioxide may be used as a war gas. 

C. Pathology .— Nitrous fumes, like phosgene, so damage the bronchioles and 
alveoli of the lung that pulmonary edema with progressive anoxemia and hemo- 
concentration develops. Inflammatory changes of the upper respiratory tract 
also are produced but are moderate. Bacterial bronchopneumonia or peribron¬ 
chial fibrosis may be sequelae. In the brain, hyperemia and multiple small 
hemorrhages are common in fatal cases. Continued exposure to nitrous fumes 
may lead to chronic inflammation of the mucous membranes of the eyes and 
upper respiratory tract. 

D. Symptoms. —When inhaled, nitrous fumes may cause little or no discom¬ 
fort. There may be coughing or choking, possibly followed by headache, 
nausea, and vomiting. In some patients central nervous system symptoms pre¬ 
dominate. After a latent period of variable length, the signs and symptoms 
associated with increasing pulmonary edema and anoxemia may appear. 

E. Diagnosis .— The diagnosis is made from the history, the symptoms de¬ 
scribed and sometimes from the pungent odor or the yellow discoloration of 
the exposed mucous membranes. 

F. Treatment. —Treatment of casualties with symptoms of pulmonary irrita¬ 
tion is the same as that outlined for phosgene poisoning. (See par. 5 D, page 
4.) The few cases with symptoms referable to the central nervous system 
either die quickly or on removal to fresh air recover spontaneously. 

G. Prognosis. —Fatal cases usually die within 48 hours. Bronchopneumonia 
and varying degrees of pulmonary fibrosis and emphysema often follow re¬ 
covery from the acute stage. 


7 







SECTION III 

VESICANTS 


9. GENERAL 

A. 1 he vesicants act primarily on the eyes and skin. In addition, they dam¬ 
age the respiratory tract when inhaled and when absorbed, they cause systemic 
poisoning. 1 he nitrogen mustards and the arsenical vesicants are the most 
dangerous in this last respect. 

B. Vesicants poison food and water, and render other materials dangerous 
to handle. 

C. Casualties contaminated with vesicants endanger unprotected attendants. 
Those in contact with such patients should wear gas masks, impermeable aprons 
and gloves, and other protective clothing if the area is contaminated. Exposed 
areas of the skin should be covered with protective ointment. 

D. Special precautions must be taken in receiving contaminated casualties to 
prevent injury of others. These casualties should be undressed in the open 
to prevent vapor accumulation indoors. They should be kept separate from 
uncontaminated patients until decontamination is complete. Contaminated 
litters, blankets and equipment should be left outdoors. It is necessary to decon¬ 
taminate equipment and ambulances after transporting such casualties. (See 
section XI, page 53 and section XV, page 69.) 

E. Identification of the agent is essential in order to apply specific treatment. 

F. The gas mask protects only the face, eyes and respiratory tract. The eye 
shield protects the eyes from contamination by liquid, but not from vapor. 
Permeable protective clothing protects the wearer from field concentrations of 
vapor and droplets of liquid vesicant for a limited period. Large drops of 
blister gas exhaust the impregnite in the clothing at the point where the 
liquid wets the fabric and some of the agents will then penetrate to the body of 
the wearer. Ointment Protective S-461 or S-330 prevents mustard gas from 
reaching the skin covered by the Ointment. 

G. After exposure without adequate protection, immediate self-aid is essen¬ 
tial .— (1) Self-Aid is the individual responsibility of all hands in all branches 
of the Navy and Marine Corps and must be accomplished immediately after 
contamination if battle conditions permit. Only casualties who are physically 
unable to decontaminate themselves are cared for by medical personnel. 

(2) If exposed to vapor, the gas mask must be put on at once. 


9 


(3) If splashed by liquid vesicant, Self-Aid is as follows: 

a. Decontaminate at once. Do not expect or wait for help from others. 

b. Speed is essential. The imperative need of prompt action cannot be 
overstressed. Correct decontamination of the eyes and skin during the first 
minute is always successful. After two minutes in the eye and three minutes on 
the perspiring skin or five minutes on the cool dry skin, no method of decon¬ 
tamination will prevent serious injury. 

c. Decontamination should be performed, however, no matter how late, 
as long as liquid mustard is still present. On the other hand, decontamination 
is of no value after vapor exposure. 

d. Vapor inhaled from splashes on the skin or clothing will damage the 
trachea, bronchi and lungs. This means every effort should be made to avoid 
breathing the fumes. 

e. All decontamination must be completed as rapidly as possible, in fact 
within the first five minutes if injury is to be avoided. 

10. MUSTARD (H) 

A. Properties .—Mustard is an oily liquid slightly soluble in water, more in 
fats and oils, and freely in gasoline, kerosene, acetone, carbon tetrachloride, and 
alcohol. These solvents do not destroy mustard. It is slowly absorbed by 
rubber gloves and rubber clothing, and so may contaminate the inner surfaces 
of these articles. Its odor is like garlic or horseradish. Mustard disappears 
slowly through evaporation and hydrolysis in moist ground. It can be de¬ 
stroyed rapidly by decontaminating chemicals and by boiling. The persistence 
of hazard from the liquid agent or its vapor depends upon the degree of 
contamination, the character of the contaminated material, the climatic condi¬ 
tions, and whether a vessel is underway or at anchor. Examples of persistence 
are given in the following table for average summer weather on open grassy 


Degree of Contamination 

Pounds of H per square 

100 by 100 yd. 

Can be 
traversed 
after 

Can be 
occupied 
after 

1,000 lb. 

6-18 hr. 

4-5 days. 

250 lb. 

1-6 hr.. 

1-2 days. 

25 lb. 

Immediately. 

1 day. 


The table assumes the wearing of the service uniform (not impregnated) 
and no anti-gas precautions. The above estimates are for average open ground 
and would be multiplied by factors of two or four for wooded areas. In winter 


10 















the persistence is two to five times as long as in summer. All values of per¬ 
sistence times are estimates and should be checked by gas detection devices 
such as paper, crayon and paint detectors. 

B. Eyes .—(1) Pathology, symptoms and prognosis. —a. The eye is more 
vulnerable to mustard than either the respiratory tract or the skin. Eye lesions 
follow an exposure of 2 hours to a concentration barely perceptible by odor. 
(0.001 mg. per liter.) This exposure does not affect the respiratory tract or 
skin. (Plate No. 7.) 

b. A latent period of 2 to 36 hours follows mild exposure, after which 
there is lacrimation and sensation of grit in the eyes. The conjunctivae and 
lids become red and edematous. Heavy exposure irritates the eye after a latent 
period of minutes to hours, and produces more severe lesions. Mustard burns 
of the eye may be divided into the following groups: 

a. Mild conjunctivitis: (75 percent of all Mustard eye cases in World War 
I). Recovery, 1-2 weeks. 

h. Severe conjunctivitis: (15 percent of cases). Blepharospasm, and 
edema of lids and conjunctivae; orange-peel roughening of the cornea. Re¬ 
covery: 2-6 weeks. 

c. Mild corneal involvement: (10 percent of cases). Areas of corneal 
erosion staining green with 2 percent of fluorescein. Superficial corneal scarring 
and vascularization. Iritis with a tendency to temporary relapses. Con¬ 
valescence requires 2-3 months. This group requiring Base Hospital care. 

d. Severe corneal involvement: (0.1 percent of cases). Ischemic necrosis 
of conjunctivae. Dense corneal opacification with deep ulceration and vasculari¬ 
zation. Convalescence requiring several months. Predisposition to late re¬ 
lapses. 

(2) Decontamination of the eyes. —Liquid mustard in the eye demands im¬ 
mediate irrigation at the earliest possible moment since irrigation is markedly 
effective in the first few seconds and worthless after two minutes. The eye 
must be flushed with water from the canteen or other uncontaminated source. 
The head is thrown back, the injured eye held open with the fingers and water 
poured slowly into it. The eye should be rolled about during the washing, 
which should be continued at least 30 seconds and not over two minutes. 
Irrigation must be completed before the gas mask is put on in spite of exposure 
to field concentrations of vapor. 

(3) Decontamination of eyelashes and lids. —The lids, lashes and skin areas 
close to the eyes are best decontaminated by washing with soap and water. 
Ointment protective is irritating to the eyes, and therefore should not be used. 
If water is not available, liquid vesicants may be removed from the lids by 
dabbing carefully with a cloth or other absorbent. 

(4) Treatment of mustard conjunctivitis. —a. Mild lesions require little 
treatment. Although they seldom become infected, 2 drops of 3 percent sodium 


U 


sulamyd solution, where available, should be instilled every 4 to 8 hours. In 
addition, Butyn Ophthalmic Ointment or Solution Anesthetic may be instilled 
for added comfort. Local anesthetics should not be used unless necessary and 
then not oftener than every 6 hours. If the lids tend to stick together during 
sleep, sterile petrolatum should be applied to the lid margins. 

b. Mustard conjunctivitis with edema of the lids severe enough to obstruct 
vision is alarming to the patient. The lids should be gently forced open to 
assure the casualty that he is not blind. Pain may be allayed by Butyn Ophtal- 
mic Ointment or drops of Solution Anesthetic. To prevent infection, a 
sulfonamide ophthalmic ointment 1 or a few drops of 3 percent to 10 per¬ 
cent solution of sodium sulamyd, where available, may be instilled every 4 
hours, after the first 24 hours. Wherever possible, sulfonamide drugs in solu¬ 
tion are preferable to ointment if the drops can be put in every 1 to 2 hours. 
The eyes must not be bandaged nor the lids allowed to stick. The accumu¬ 
lation of secretions in the conjunctival sac or any pressure on the eye at this 
stage predisposes to corneal ulceration. Irrigations must be held to the mini¬ 
mum necessary to dislodge secretions, since excess fluid and trauma loosen 
the injured corneal epithelium. Isotonic or slightly hypertonic sterile solutions 
must be used, never hypotonic solutions; 1 percent saline is satisfactory. When 
the lids can be opened sufficiently for an ophthalmic examination, the cornea 
should be stained with fluorescein, one drop of 2 percent solution in saline into 
the lower conjunctival sac. The eye then should be rinsed with a few drops 
of sterile saline and examined for yellowish-green staining of the cornea. Stain¬ 
ing indicates a loss of corneal epithelium. If the cornea stains, or if iritis or 
photophobia is present, atropine should be administered in 1 percent solution. 
The patient is then transferred to the care of the ophthalmologist. Sealing 
of the lids may be prevented by the application of petrolatum to the lid 
margins. Dark glasses or an eye shade should be worn for photophobia, but 
discarded as soon as possible) to prevent developing of neurasthenia. 

t (5) Treatment of infected mustard burns of the eye. —a. Secondary infection 
is serious. Secretions must be removed gently by a minimum of irrigation with 
1 percent saline. The eye should then be filled with a sulfonamide ophthalmic 
ointment 1 every 4 hours or a 10 percent solution of sodium sulamyd, where 
available, every 2 hours. Irrigation should be employed only to remove the 
accumulated exudate. Local anesthesia should not be used unless necessary, 
and then not oftener than every 6 hours. It is very important to prevent 
sticking of the lids and the sealing in of purulent secretions. Cases develop¬ 
ing corneal ulcer or other complications should be referred to the opthal- 
mologist. 


1 Sulfonamide Ophthalmic Ointment: 5 per cent Sodium Sulfadiazine in 50 percent 
each of Lanolin and Petrolatum. 


72 



C. Skin .— (1) Pathology. —a. The severity of the lesions and the rapidity 
with which they develop are greatly influenced by weather conditions as well 
as by the degree of the exposure. Hot, humid weather, as in the tropics, 
strikingly increases the action of mustard. Even under temperate conditions, 
the warm, moist skin of the perineum, external genitalia, axillae, antecubital 
fossae and neck are particularly susceptible (Plate No. 2).- Cold weather and 
snow delay the action of mustard. 

b. After a latent (Plate No. 1) period of variable length, an erythema gradu¬ 
ally appears, resembling sunburn. Vesication may follow. Usually multiple 
pinpoint lesions form and coalesce into a single large vesicle (Plate No. 3). 
The typical blister is very superficial, translucent and surrounded by erythema. 
The blister fluid is clear, straw-yellow and does not coagulate early. It is non¬ 
vesicant. 

c. The amount of dermal edema is variable (Plate No. 2). In severe burns 
it may be considerable, and limit motion of a limb. Large drops of liquid 
may produce a ring of vesicles surrounding a gray-white area of skin which, 
though necrotic, does not vesicate. If a blister is not ruptured, it begins to be 
resorbed in about a week. The roof forms a crust, beneath which re-epidermi- 
zation takes place. The vesicles frequently break, however, and infection may 
occur. 

d. Mustard burns usually are followed by a persistent brown pigmentation, 
except at the site of actual vesication, where there may be a temporary de¬ 
pigmentation (Plate No. 4 and Plate No. 5). 

e. Repeated burns may lead to hypersentitivity of the skin to mustard. 

(2) Symptoms and prognosis. —a. Exposure of the skin is followed by a 
symptomless latent period of hours or days which varies in length with the 
degree of contamination. In temperate weather this period usually lasts 6 to 
12 hours, and in tropical weather 1 to 3 hours. As lesions appear, the skin 
develops generalized itching, which may last 4 to 8 days or longer. Blisters 
usually appear within 18 to 36 hours. The uncomplicated mustard lesion heals 
without scarring, usually in 3 to 6 weeks. 

(3) Diagnosis of skin lesions due to mustard. —a. Nearly identical skin 
lesions are produced by mustard and the nitrogen mustards. Mustard burns 
tend to resemble those due to lewisite and other arsenical vesicants. Differen¬ 
tiation of mustard lesions from those produced by lewisite is based upon: 

a. History of exposure to the gas. 

h. Absence of pain or discomfort at time of contamination (lewisite causes 
immediate pain). 

c. Latent period before the development of symptoms (none with lewisite). 

d. Wide zone of erythema surrounding blisters (not prominent in the case 
of lewisite). 

13 

t 


PLATE NO. 1 


Early Mustard Erythema 

The casualty clothed in a defective impregnated protective 
suit was exposed to Mustard vapor concentration of 17 
mg/cu. meter for 60 minutes. One hour after exposure 
the skin itched and burned. The picture shows the intense 
generalized mustard erythema. Note its absence about the 
ankles and feet which were protected by 2 pairs of socks 
and a pair of overshoes. The case demonstrates the in¬ 
sidious way in which mustard gas injures its victim. Since 
the action is delayed the gas may continue to inflict injury 
for hours before the victim recognizes its presence. 


PLATE NO. 2 

Mustard Burn of Genital Organs 

Same casualty as presented in plate No. 1. It illustrates 
the extreme vulnerability of the genitals to burns by blister 
gases. Other moist regions are equally sensitive. Note 
the raw and swollen scrotum and penis and contrast with 
the thighs which are only erythematous. Burns of the 
genital organs are painful and interfere seriously with 
wearing of clothes and with walking. 










PLATE NO. 3 

The Blisters of a Mustard Burn 

This picture presents a severe mustard burn of the neck 
after exposure to mustard vapor concentration of 20 
mg/cu. meter for 30 minutes. Blistering began 24 hours 
later and the picture was taken 4 days after exposure. The 
mustard blister is usually a clear tense bleb with slanting 
sides. Note the pinpoint vesicles about the large blister. 


I 


PLATE NO. 4 

Severe Mustard Vapor Burn 

The casualty clothed in a defective charcoal coated pro¬ 
tective suit was exposed on two successive days to Mustard 
vapor concentration of 20 mgjcu. meter for 60 minutes. 
The suit was worn for 56 hours thereafter and then re¬ 
moved because of developing erythema of the buttocks, 
thighs and genital organs. Subsequently the erythema of 
the buttocks beca?ne very intense. Edema and blisters ap¬ 
peared. The picture, taken eleven days after the second 
exposure to the vapor, shows the violaceous erythema of 
the buttocks. Note the scattered irregular areas of super¬ 
ficial ulceration where the skin has denuded. The blisters 
that develop in these burned areas are almost painless, but 
the raw surfaces left after the blisters burst are acutely 

sensitive. 


\ 


PLATE NO. 5 

Mustard Vapor Burn in Brown Pigmented Stage 

Same casualty as presented in plate No. 4 but 9 days later, 
or 20 days after the second exposure to the vapor. The 
case now presents the brown pigmentation which occurs in 
mustard burns. This gradually deepening pigmentation 
usually appears in areas that were first inflamed and red, 
but it may arise without such preceding erythema. It may 
begin to appear at any time from the fifth day onward 
and it persists for several weeks until the stained cuticle 
desquamates. There is no deep pigmentation and the sites 
of actual blistering usually are temporarily depigmented. 




















I 














It should be remembered that vesicular lesions much like mild mustard burns 
may be produced in sensitive individuals by a variety of substances, notably 
plant poisons such as poison ivy or poison oak. 

(4) Decontamination of the skin. —a. The contaminated skin should be 
blotted quickly with the absorbent paper furnished with the protective ointment 
or with a dry cloth. (Later destroy the used absorbent material.) 

b. Ointment Protective S—46l or S—330 2 should then be squeezed onto the 
spot on the skin and thoroughly rubbed into the affected areas with the fingers 
for about 15 seconds. Excess ointment should then be wiped off. On large 
splashes, the ointment should be applied and removed once more. 

c. If reddening of the skin has appeared, cleanse the area with soap and 
water. Ointment Protective S-461 or S-330 is irritating to the reddened skin 
and should be used only when liquid mustard is still present and soap and 
water are not available for thorough washing. Solvents for removal should not 
be used if soap and water are available. 

d. Should the supply of Ointment Protective run short, the following alter¬ 
natives may be employed: 

a. Bleach paste: Prepared by mixing 1 part of bleach and 2 parts of water. 
Because of its irritant properties, it must be washed off the skin within three 
minutes. 

b. Solvents: Any nonirritant organic solvent may be used in an emergency 
to dissolve and dilute the liquid mustard. Since solvents do not neutralize the 
vesicant, the mustard solution formed must be completely and rapidly removed 
from the skin by flooding with a large excess of the solvent. Alternatively, 
the area may be sponged repeatedly with cotton or gauze dampened with solvent 
with care to avoid the spread of mustard from contaminated skin. Gasoline, 
kerosene, alcohol and carbon tetrachloride (from automobile fire extinguishers) 
are most commonly available. Caution ; Precautions against fire and explosion 
must be observed when employing inflammable solvents. Leaded gasoline and 
carbon tetrachloride, when absorbed by the body, are poisonous. 

c. The decontaminated skin areas should be thoroughly washed with soap 
and water as soon as practicable after decontamination. 

d. Wounded personnel, with liquid mustard contamination of the skin will 
seldom be received at battle dressing stations on ships or at shore medical 
installations in time to prevent subsequent blistering. Nevertheless, if ery¬ 
thema has not appeared, known or likely areas of contamination should be 
decontaminated as outlined in the preceding paragraph. 

(5) Decontamination of hair. —a. The contaminated hair may be decon¬ 
taminated with bleach paste or clipped off. The scalp should then be washed 
with soap and water. Ointment Protective may be used but is difficult to apply 
and to remove. 


2 An individual issue of Ointment Protective is made to all men in combat zones. 

17 



(6) Treatment of mustard erythema. —a. Mustard erythema in mild cases 
requires little or no treatment. If annoying itching is present, considerable 
relief can be obtained by covering the area with anesthetic ointment or with 
calamine lotion. 3 Severe erythema is often accompanied by edema, stiffness 
and pain. Effective subjective relief and subsidence of edema may be obtained 
in these cases by application of a light dressing moistened with saline or with 
amyl salicylate 4 , where available. The dressing is remoistened every 12 to 24 
hours for about four days. Painful erythema of the genitalia may be treated 
with calamine lotion and a suspensory bandage applied. Alternatively, petro¬ 
latum, a light protective dressing and a suspensory may be used. 

(7) Treatment of the mustard blister. —a. Large blisters, if tense or painful, 
should be drained by puncture at the lower margin, after sponging the area 
with alcohol. It is not necessary to express clots; they will be absorbed and 
not delay healing. Blisters are often partially refilled with fluid 24 hours after 
drainage when a second puncture may be desirable to prevent traumatic rupture 
and a loss of blister top. Usually the blister may be covered with a dressing 
which can be moistened once or twice daily with saline or with amyl salicylate 4 , 
where available, if there is pain or itching. Thereafter, a dry or a sterile 
petrolatum dressing may be used. Frequent dressings are not desirable. 

b. If the dressing sticks to the wound, care will be necessary to avoid 
pulling off the blister top. It is good practice to trim the edges of the 
adherent gauze, leave it in place, and put a fresh dressing over it. If necessary 
to examine the wound or treat infection, the dressing can be soaked off. 

c. Small blisters may be covered simply with a light dry dressing, moistened 
once daily for 3 or 4 days with saline or with amyl salicylate 4 if the burn is 
painful or itches. The dressing can be removed ordinarily in 2 or 3 weeks, 
when the area will be covered by a thin, pliable crust. 

(8) Treatment of denuded areas. —a. Blistered areas which have become de¬ 
nuded may be coated with 5 percent Ointment sulfathiazole (See par. 10 
C(9), page 19). 

b. Alternatively, sterile petrolatum may be used, as for thermal burns. (See 
section X, page 49.) 

c. Strong antiseptics and escharotics of all kinds are contraindicated. 

d. Sterile technic should be employed, if possible including face masks for 
attendants as for thermal burns. Frequent change of dressings is to be avoided. 

e. Occasional extensive granulating surfaces may require skin grafting. Mul¬ 
tiple pinch grafts have proved successful. 

J Calamine lotion, NF., with 0.5 percent each of phenol and menthol. 

. 4 Caution: The strong odor of amyl salicylate may put the soldier at a disadvantage 
m close jungle fighting as the odor may assist the enemy in stalking him, especially 
at night. Amyl salicylate should not be used in the axillae, groin, perineum or about 
the genitalia. 


18 




(9) Treatment of infected mustard burns:- —a. Contamination of mustard 
burns with saprophytic bacteria is common, but not serious. If there is no in¬ 
flammatory reaction, the treatment is the same as for uncontaminated burns. 
(See par. IOC (6) & (7), page 18.) 

b. Infected burns with an inflammatory reaction should be considered in¬ 
fected wounds. They may be treated with sulfathiazole ointment. The latter 
should be limited to 100 grams of 5 percent ointment and to not more than 
5 percent of the body surface, since there is danger of excessive absorption of 
the sulfonamide. Infection is best controlled by orai administration of a sul¬ 
fonamide. Sulfadiazine or sulfanilamide may be given, 4 grams (grains 60) 
initially and 1 gram (grains 15) every 4 hours thereafter. Sufficient fluids 
should be given to maintain output of urine over 1500 c.c. (11/? quarts) daily. 
Two grams (grains 30) of sodium bicarbonate may be given every 4 hours to 
keep the urine alkaline. 

c. Strong local antiseptics are contraindicated. 

D. Respiratory Tract .— (1) Pathology. —a. Inhalation of mustard vapor 
causes irritation of the mucous membranes of the respiratory tract. Inflamma¬ 
tory changes may include necrosis with pseudomembrane formation and slough. 
A cast of the tracheobronchial tree may be formed. 

b. The pulmonary parenchyma, injured by mustard vapor, shows patchy 
emphysema, congestion and atelectasis. These changes are insufficient to cause 
anoxia, but they may be complicated by bronchopneumonia which is respon¬ 
sible for almost all the deaths following mustard. The mortality from mustard 
in the American Expeditionary Force in World War I, slightly more than 2 
percent, resulted almost entirely from inhalation of vapor. 

(2) Symptoms and prognosis. —a. Respiratory tract lesions, like skin in¬ 
juries, develop slowly and do not reach maximal severity for several days. 
Symptoms begin with hoarseness, which may progress to aphonia. A cough 
appears early and becomes productive. Fever, dyspnea, and moist rales may 
develop. The incidence of bronchopneumonia is high. Convalescence is slow, 
and cough may persist a month or longer. Milder symptoms, like hoarseness, 
last only a week or two. 

(3) Treatment of injury of respiratory tract due to mustard. —a. Mild res¬ 
piratory tract injury with hoarseness and sore throat only, usually requires no 
treatment. Cough may be relieved by codeine and pharyngitis with alkaline 
gargles. Relief from nasal inflammation may be obtained with nose drops of 
anesthetic solution. Since severe respiratory tract injuries predispose to bron¬ 
chopneumonia, the prophylactic oral administration of sulfadiazine or sulfa¬ 
nilamide, 2 grams (grains 30) initially and 1 gram (grains 15) every 6 hours 
thereafter, is indicated. (See par. 5D(6), page 5.) Laryngitis and tracheitis 
should be treated by steam inhalations. Morphine or the barbiturates can be 


19 


used to quiet the patient. Secondary bronchopneumonia should be treated like 
any other bronchopneumonia. 

E. Systemic and Gastrointestinal .—(1) Symptoms. —a. Severe exposure of 
the skin to mustard may cause transient nausea and vomiting. The systemic 
reaction from large mustard burns is like that from thermal burns of compar¬ 
able size. 

b. Ingestion of food or water contaminated by liquid mustard produces pain, 
diarrhea and prostration. Mustard vapor does not significantly contaminate 
food or water. 

(2) Treatment. —a. Atropine may prove useful in reducing the gastroin¬ 
testinal activity. Injury due to the ingestion of liquid mustard in food or 
water may require morphine and atropine for the relief of pain, and shock 
therapy for collapse. Bismuth subcarbonate (or subnitrate') can be used for 
diarrhea. 

(3) Prognosis. —a. A few deaths are recorded from the systemic effects of 
mustard absorbed through the skin in extensive burns. These casualties showed 
pronounced leukopenia, which may be regarded as a bad prognostic sign. 

b. Severe injury from ingestion of mustard is rare. 

11. NITROGEN MUSTARDS (HN) 

A. General. The nitrogen mustards are oily, colorless or pale-yellow liquids, 
sparingly soluble in water but freely soluble in organic solvents. Some possess 
a faint fishy odor, while others are odorless. Their volatility varies with the 
particular compound. All are persistent, though not equally so. They are 
more readily hydrolyzed than mustard, but less so than lewisite. All their 
hydrolytic products, except the final ones, are toxic. 

B. Eyes .—(1) Symptoms and pathology. —Nitrogen mustards irritate the 
eyes before the skin or respiratory tract. The eye irritation caused by the nitro¬ 
gen mustards appears in a shorter time than that from mustard but not as early 
as that from lewisite. Mild or moderate exposure causes mild smarting and 
lacrimation within 15 minutes. Thereafter symptoms may wax and wane until 
they become persistent about 2l/ 2 hours later and reach their maximum in 8 to 
10 hours. After more severe exposure, symptoms may begin immediately and 
progress for 24 hours or longer. Mild exposure produces erythema and edema 
of the palpebral and bulbar conjunctivae and superficial steamy haziness of the 
cornea. Irritation, lacrimation, deep eye pain, miosis and photophobia are 
usually present. After more severe exposure the symptoms described above are 
followed by spotty hemorrhagic discolorations of the iris. The corneal epithe¬ 
lium begins to show a roughened, lusterless surface with areas of punctate stain¬ 
ing demonstrable by the instillation of fluorescein. Severe exposure may cause 
the corneal epithelium to exfoliate. Slit lamp examination will reveal clouding 
and edema of the corneal substance extending deep below Bowman’s membrane. 
Local necrosis of the cornea may rupture the globe. 


20 


(2) Decontamination and treatment. —These are the same as for mustard. 
(See par. 10 B (2), page 11.) In general, the symptoms and the lesions are 
more severe, requiring intensive and early treatment with atropine. 

(3) Prognosis. —The prognosis in contamination with any liquid nitrogen 
mustard is serious, unless the agent is removed by irrigation within a minute or 
two. Mild injury progresses to complete recovery in about 2 weeks. Severe 
injury heals more slowly requiring 9 to 12 weeks or longer. The cornea heals 
by vascularization, and the iris with discoloration and atrophy. Scarring may be 
expected. The degree of recovery is remarkable, although relapses may occur, 
as from mustard injuries. 

C. Skin. —(1) Symptoms and pathology. —The skin is more resistant than 
other tissues to the vapor of the nitrogen mustards and is less affected by them 
than by mustard. In mild exposures there may be no skin lesions. After 
severe exposures erythema appears earlier than is the case in mustard contami¬ 
nation. Later, blisters may appear in the erythematous areas. Liquid nitrogen 
mustards are also vesicant. The blisters produced are more superficial and 
more rapidly formed, but are otherwise similar to those caused by mustard 
(Plate No. 6). 

(2) Decontamination and treatment. —The contaminated areas should be 
washed with large quantities of soap and water or water alone. If soap and 
water are not available, decontamination procedures are the same as for mustard. 
(See par. 10 C (4), page 17.) It should be remembered however that oint¬ 
ment protective merely dilutes the nitrogen mustards and does not destroy them. 
It is necessary, therefore, to wash off the film of ointment with water or soap 
and water as soon as possible. The possibility of systemic poisoning from 
absorbed nitrogen mustards through the skin is much greater than with liquid 
mustard. Decontamination should be carried out as late as 2 to 3 hours after 
exposure, in an attempt to neutralize the nitrogen mustard not bound as yet by 
the skin, even at expense of increasing somewhat the severity of the local reac¬ 
tion. Later treatment of skin lesions is like that for mustard burns. (See par. 
10 C (6), (7), (8) and (9), pages 18 and 19.) 

(3) Prognosis.— Most blistered areas will heal in 2 to 4 weeks if infection 
is prevented. Occasionally, deeper burns require a longer time. 

D. Respiratory Tract. —(1) Pathology. —The lesions caused by nitrogen 
mustards are similar to those caused by mustard. They decrease in severity 
down the respiratory tract from the point of entry. In the nose, larynx and 
trachea, there may be marked swelling, erythema, and necrosis of the mucosa, 
followed by sloughing, hemorrhage and fibrino-purulent exudation. The larynx 
is especially vulnerable. Edema and necrosis may lead to respiratory obstruc¬ 
tion. In sever cases the damage may extend to the bronchioles and alveoli. 
Although pulmonary edema usually is not massive, secondary pulmonary in¬ 
fection is common. 


21 


PLATE NO. 6 

Nitrogen Mustard Burn 

A Nitrogen Mustard burn of the fingers was accidentally 
incurred by a research worker in handling metal rods which 
were used to inflect experimental burns. He wore surgical 
rubber gloves and was not aware that Nitrogen Mustard 
had penetrated them until he noticed a burning sensation 
10 hours after handling the rods. This is the appearance 
of the burn the following morning. A large blister fills 

the inter digital space. 














' 

i ■ m '. ■ 1 - * • 11 















(2) Symptoms. —The symptoms are much the same as those due to mustard, 
namely, delay in appearance, irritation of the nose and throat, hoarseness pro¬ 
gressing to aphonia, a persistent cough, evidence of lung edema. Broncho¬ 
pneumonia may appear after the first 2 to 4 hours. 

i 

(3) Treatment. —The treatment of casualties with respiratory tract involve¬ 
ment is the same as for mustard. (See par. 10 D (3), page 19.) 

(4) Prognosis. —Mild tracheitis is likely to result in a cough which persists 
for several weeks. The prognosis is grave if there is severe respiratory tract 
involvement. Most late deaths are due to pneumonia. 

E. Gastrointestinal tract. —(1) Following oral introduction or systemic ab¬ 
sorption, the nitrogen mustards cause injury to the intestinal tract. Lesions are 
most marked in the small intestine and consists of inflammatory and degenera¬ 
tive changes in the mucosa. In animals, severe diarrhea, which may be 
hemorrhagic, occurs. In man, the ingestion or parenteral administration of 
2 to 6 mgm. causes nausea and vomiting. 

F. Systemic effects .—(1) Pathology. —The most specific effects of the nitro¬ 
gen mustards are on hematopoietic and lymphoid tissue. These follow ab¬ 
sorption from intact skin, respiratory or gastrointestinal tract. In bone marrow 
the degenerative changes can be detected within 12 hours and may progress to 
severe aplasia. The thymus, spleen and lymph nodes involute rapidly with 
necrosis and phagocytosis of their lymphocytes. This injury is demonstrable 
in the blood through a transient leukocytosis of a few hours’ duration followed 
by severe lymphopenia, granulocytopenia, thrombocytopenia and a moderate 
anemia. The blood picture may show little change for 5 to 10 days after 

exposure, at which time the white count may fall below 500 cells/mm3. The 

\ 

various nitrogen mustards differ in their abilities to produce these changes. 

(2) Treatment. —The blood should be studied carefully and transfusions of 
whole blood given for thrombocytopenia or anemia. Vomiting or severe diar¬ 
rhea may call for the replacement of fluid in addition to symptomatic treatment 
with sedatives, atropine and opiates. If these symptoms are prolonged, every 
attempt should be made to maintain an adequate nutritional status by intra¬ 
venous infusion of glucose, amino acids and plasma, and the parenteral admin¬ 
istration of vitamins. 

(3) Prognosis. —Leukocyte counts below 2,000 and great loss in weight 
probably point to a fatal outcome. 

(4) Diagnosis. —Diagnosis is based upon a history of exposure, a faint fishy 
odor on the skin and clothing, and signs and symptoms characteristic of mus¬ 
tard exposure but which appear more rapidly than with mustard. 


23 


PLATE NO. 1 , EXPLANATION 

Burns of the Eye , With Blister Gases 

It is not possible to photograph many human eyes burned severely by blister gas. How¬ 
ever severe lesions can be produced experimentally in animals to demonstrate many 
characteristics of the severe blister gas lesions of the human eye. The rabbit eye 
though less sensitive than the hutnan eye is nearly comparable. 

Photo No. 1: A perfectly normal rabbifs eye. Note the complete absence of any 
redness or infection of the conjuctiva, the sparkling clear cornea and the smooth bright 

iris. 

Photo No. 2: A rabbit’s eye six hours after exposure to a saturated mustard vapor 
at 23 degrees centigrade for only one minute. The nictitating membrane and the 
palpebral conjunctiva are mildly swollen and infected. The light reflex on the cornea 

is slightly blurred. Compare with photo No. 3. 

Photo No. 3: Twenty-four hours after injury the conjunctiva is strikingly sivollen and 
injected and there are ?nany small hemorrhages scattered through the reddened areas. 
There is a diffuse haziness of the cornea. Thick mucopurulent secretion can be seen 
clinging to the margin of the upper lid and on the matted hair belou' the eye. The 
pupil was jnoderately contracted dtie to an associated iritis. The cornea showed areas 
of punctate staining when 2 percent fluorescein was applied. Compare with Photo No. 6. 

Photo No. 4: Twelve days after injury the edetna of the conjunctiva has subsided. 
The nictitating membrane is still injected and swollen. The corneal damage has 
progressed as evidenced by distortion and the development of a large bulla. The use¬ 
fulness of this eye has been destroyed and it will probably rupture in a day or tivo. 

Compare with Photo No. 7 . 

Photo No. 3: A rabbit’s eye only one hour after exposure to a saturated lewisite 
vapor at 23 degrees centigrade for 30 seconds. An extreme degree of conjunctival 
edema has developed, obscuring the cornea. The rapid onset of eye injury due to 
lewisite is striking contrast to the delayed slow development following exposure to the 
vapors of mustard or the nitrogen mustards. Compare with Photo No. 2. 

Photo No. 6: Two days after exposure the conjunctival edema has partially subsided. 
A large amount of mucopurulent discharge fills the conjunctival sac. The cornea showed 
a well delineated area cotnpletely denuded of epitheliutn. The iris was hyperemic and 
thickened and its normal pattern was further blurred by corneal haziness and exudate 
in the anterior chamber. Compare with Photo No. 3. 

Photo No. 7: Eleven days after exposure the injection and edema has subsided. There 
is considerable mucopurulent discharge present. The cornea is now opaque because 
of the dead white necrosis of the bulbar conjunctiva. It was impossible to see the iris 
and the anterior chamber. This eye will perforate in a few days and be completely 

destroyed. 


24 

















































































































12. LEWISITE (L) 

A. General. —(1) Lewisite is an oily, colorless to light amber liquid with 
a faint odor of geraniums. It is more volatile and less persistent than mustard, 
making it more effective in cold weather. Lewisite is readily soluble in gas¬ 
oline, kerosene and alcohol. Although poorly soluble in water-, it is rapidly 
hydrolyzed in contact with moisture. Lewisite oxide, one of the hydrolysis 
products, is vesicant and toxic and may contaminate ground for long periods. 
Lewisite, like mustard, penetrates fabrics and rubber, making it dangerous to 
wear clothing or rubber gloves previously contaminated. 

(2) Lewisite, like mustard, injures the eyes, skin and respiratory tract, and 
may produce systemic effects. Liquid lewisite in contrast to liquid mustard 
causes stinging pain in 10 to 30 seconds, which increases in severity. How¬ 
ever, the risk of burns from field concentrations of vapor is small. No decon¬ 
tamination or treatment is necessary following exposure to vapor unless pain is 
experienced. Then the procedures to be followed are those to be described 
under liquid lewisite. (See par. 12 B (2), (3) and (4), page 25; par. 12 C 
(4) to (11), page 27.) 

B. Eyes .—(1) Symptoms, pathology atid prognosis .—Liquid lewisite causes 
severe damage to the eye. On contact, pain and blepharospasm appear instant¬ 
ly. Edema of the conjunctiva and lids follows rapidly and closes the eye in an 
hour (Plate No. 7). Inflammation of the iris usually is evident by this time. 
After a few hours the edema of the lids begins to subside, while haziness of the 
cornea develops and iritis increases. The corneal injury, which varies with the 
severity of the exposure, may heal without residue, may develop pannus forma¬ 
tion, or progress to massive necrosis. The iritis may subside without permanent 
impairment of vision if the exposure was mild, or after heavy exposure, hypo¬ 
pyon may ensue, terminating in necrosis, depigmentation of the iris and syne- 
chiae formation. Liquid lewisite instantaneously produces a gray searing of the 
cornea like an acid burn at the point of contact. Necrosis and sloughing of 
both bulbar and palpebral conjunctivae may follow very heavy exposure. All 
injured eyes are susceptible to secondary infection. Mild lewisite conjunctivitis 
in man heals in a few days without specific treatment. Severe exposure may 
cause permanent injury or blindness. 

(2) Decontamination of the eyes .—Eyes contaminated with liquid lewisite 
required immediate treatment with Ointment BAL. If BAL is used the first 
minute following contamination, the eye usually recovers in a few days. When 
used 10 minutes after contamination, the lesion requires several weeks to heal 
and ordinarily leaves permanent damage. Ointment BAL exerts little influence 
after 30 minutes. Ointment BAL is available to all men. It is issued in a 
1/? oz. tube and is to be carried in the gas mask carrier. 

(3) Procedure of Decontamination with Ointment BAL .—a. Open the tube 
of BAL ointment. 


25 


b. If the eye can be opened by traction on the lower lid with the fingers, 
squeeze the ointment directly into the injured eye and massage the lids gently. 

c. If the eye cannot be opened, apply the ointment to the lids and rub in 
as much as possible between them. 

d. As soon as the pain lessens and the lids can be pulled apart, squeeze 
additional Ointment BAL into the eyes. 

e. Rub a small quantity on the lashes, lids and skin around the eyes. 

(4) Caution. —a. BAL ointment should not be put into the eye unless there 
is acute pain. BAL causes sharp stinging pain and blepharospasm in the normal 
eye. The discomfort lasts about 30 minutes, followed by irritation and redness 
for several hours. BAL has the opposite effect in eyes contaminated with 
lewisite, giving marked and rapid relief from pain. When the identity of the 
contaminating agent is in doubt, it is advisable to use BAL for any acutely 
painful war gas contamination of the eye. 

b. Hydrogen peroxide solutions must not be used in the eye; they are worth¬ 
less for the treatment of lewisite injury and are damaging to the cornea. 

0) Treatment of lewisite conjunctivitis. —The treatment is like that for 
mustard. (See par. 10 B (4) and (5), pages 11 and 12.) 

C. Skin .—(1) Symptoms. —Stinging is felt in 10 to 30 seconds after con¬ 
tact with liquid lewisite. This increases in severity as the lewisite penetrates, 
and in a few minutes becomes a deep aching pain. After five minutes’ contact, 
a gray area of burned epithelium is apparent much like an acid burn. Erythema 
and edema of the skin appear in about 30 minutes. Erythema is like that caused 
by mustard but is more painful. Itching and irritation persist only about 24 
hours. 

(2) Pathology. —Liquid lewisite acts more rapidly and produces more severe 
lesions of the skin than does mustard. Lewisite vapor, however, is distinctly 
less dangerous than mustard vapor because vapor concentrations in the field are 
difficult to maintain. Contamination of the skin with liquid lewisite is followed 
in a short time by erythema. Vesication follows and tends to cover the entire 
area of erythema, so that the red peripheral halo associated with the mustard 
lesion is seldom seen. The lewisite blister, often indistinguishable from the 
mustard blister, is steep-sided with a thick roof and contains slightly opaque 
yellow fluid. Microscopically, the roof exhibits more complete necrosis than 
does that of the mustard blister, a greater infiltration of cells within the vesicle, 
and an injury extending much deeper into the corium. The vesicle fluid con¬ 
tains a trace of arsenic, but is non-toxic and non-vesicant. Blisters are often 
well developed in 12 hours and are painful at first, in contrast to the relatively 
painless mustard blister. After 48 to 72 hours the pain lessens. Deep burns 
from lewisite rarely occur in man, because the pain on contact gives warning 
in time for decontamination. Such burns probably would occur only in the 
case of an unconscious victim. Lewisite can penetrate the skin, subcutaneous 


26 


tissue, and muscle, causing enormous edema and gelatinous necrosis of the 
affected part. This is followed by failure of circulation, gangrene and slough. 

(3) Prognosis. —Lewisite erythema heals somewhat more rapidly than mus¬ 
tard erythema, and with less pigmentation. Small lewisite blisters heal in 
about the same time as those due to mustard. The larger lewisite lesions in¬ 
volve deep injuries which heal slowly and require skin grafts. 

(4) Decontamination of skin — vapor. —The risk of skin burns from field 
concentrations of lewisite vapor is small and decontamination of the skin for 
such exposure should seldom be required. When drops of liquid lewisite con¬ 
taminate the clothing, concentrated vapor from these drops penetrates the cloth 
and damages the underlying skin. Such clothing must be removed promptly. 
Decontamination of the skin may be accomplished if specific measures are taken 
within a few minutes after contact. 

(5) Decontamination of the skin — liquid. —a. The removal of liquid lew¬ 
isite from the skin is the individual responsibility, that is, a matter of self-aid 
for all personnel in all branches. 

b. If the skin is wet with lewisite, the excess liquid is quickly removed by 
blotting with absorbent material. 

c. For each blot a clean portion of the absorbent should be used and then 
discarded. Care should be taken in discarding the used absorbent to prevent 
spread of lewisite to personnel or materiel. 

d. Ointment BAL 5 is then immediately applied to area contaminated. BAL 
is a specific antidote for lewisite and other arsenicals. It should be spread on 
the skin in a thin film, rubbed in with the fingers and allowed to remain at 
least 5 minutes. Thereafter the ointment may be washed off when conditions 
permit. 

e. If Ointment BAL is not available, wash immediately with soap and water. 

f. Organic solvents are effective in preventing blisters only when used in the 
first few seconds. 

g. Ointment BAL sometimes causes temporary stinging and itching urticarial 
wheals on the skin. The lesions usually last only an hour or so and should not 
cause alarm. Mild dermatitis, persisting a few days, may follow a single appli¬ 
cation. Dermatitis is fairly frequent if repeated applications are made to the 
same skin area. This prevents the use of the Ointment BAL as a protective 
film in contrast to the use of anti-mustard ointments. 

(6) Wounded men, contaminated with liquid lewisite, will seldom be re¬ 
ceived at battle dressing stations on ships or medical installations ashore in time 
to prevent blistering. However, their burns may be lessened and significant 
systemic protection obtained if the decontamination procedures outlined under 
(5) are carried out promptly. 

•' An individual issue of Ointment BAL is made to all men in combat zones. 


27 



(7) Decontamination oj hair. —Contaminated hair may be decontaminated 
with Ointment BAL and then washed with soap and water. As an alternative, 
the hair may be clipped off followed by washing of the scalp with soap and 
water. 

(8) Treatment oj lewisite erythema. —The treatment of lewisite erythema is 
the same as that for mustard erythema, except that treatment seldom is required 
for longer than 24 hours. (See par. 10 C (6), page 18.) BAL ointment 
may be tried in the early stages. 

(9) Treatment oj the lewisite blister.- —Lewisite and mustard blisters are 
treated alike. (See par. 10 C (7), page 18.) 

(10) Treatment oj denuded areas and injected lewisite burns. —The treat¬ 
ment of these lesions is the same as that for similar lesions due to mustard. 
(See par. 10 C (8) and (9), pages 18 and 19.) 

(11) Treatment oj deep lewisite burns. —Large burns may be accompanied 
by serious systemic poisoning and shock demanding general measures as well 
as local treatment. (See par. 12 E (3), page 29.) Morphine and splinting 
of the affected parts may be necessary for the relief of pain. When the burned 
tissue becomes gangrenous, it may be allowed to slough, or it may be excised. 
(See section X, page 49.) 

D. Respiratory tract .— (1) Symptoms.- —-Lewisite vapor is highly irritating 
to the respiratory tract and quickly induces sneezing and coughing. This prop¬ 
erty and the strong smell of geraniums have so effectively warned of its 
presence, that no severe respiratory injuries have been reported. Inhaled 
lewisite vapor produces lesions of the respiratory mucosa essentially similar to 
those produced by mustard. Edema of the lung often is more marked, and is 
frequently accompanied by pleural fluid. 

(2) Treatment oj respiratory tract injury due to lewisite. —Since there have 
been no human respiratory tract injuries from lewisite, treatment is recom¬ 
mended solely from the results of animal experimentation. In general, the 
treatment is a combination of that for the systemic effects of lewisite (See par. 
12 E (3), page 29) plus that for mustard respiratory tract injuries. (See 
par. 10 D (3), page 19.) 

(3) Prognosis. —The prognosis in respiratory tract injury from lewisite is 
unknown but probably is similar to that for an equivalent mustard injury with 
the added danger of systemic arsenical poisoning. 

E. Systemic .— (1) Pathology and symptoms. —Liquid lewisite on the skin, 
as well as inhaled vapor, is absorbed and may cause systemic poisoning. A 
manifestation of this is a change in permeability which permits loss of sufficient 
fluid from the blood stream to cause hemoconcentration, shock and death. In 
non-fatal cases, hemolysis of erythrocytes has occurred with a resultant hemo¬ 
lytic anemia. Although lewisite is oxidized within the body, it may still be 


toxic. Its excretion into bile by the liver produces focal necrosis of that organ, 
necrosis of the mucosa of the biliary passages with peribiliary hemorrhages and 
some injury to the intestinal mucosa. Acute systemic poisoning from large 
burns, in animals, causes pulmonary edema, diarrhea, restlessness, weakness, 
subnormal temperature and low blood pressure. 

(2) Prognosis. —Burns severe enough to cause shock and systemic poisoning 
are dangerous to life. Even though the patient survives the acute effects, the 
prognosis must be guarded for several weeks. 

(3) Treatment. —There has been no experience in treating systemic lewisite 
poisoning in man, but the following measures may be of value: 

a. As soon as possible, apply the entire contents of one tube of BAL oint¬ 
ment to the contaminated skin, spread widely, and rub in well to obtain the 
maximum absorption. Leave the preparation on the skin. Repeat at 12 hourly 
intervals for 48 hours and daily thereafter for 4 days. 

b. If signs of shock appear, administer the usual treatment, including plasma. 

c. Give fluids freely and intravenously if necessary. 

d. Give a high carbohydrate, high protein diet, employing intravenous glu¬ 
cose if the patient cannot retain food by mouth. 

e. Give supplementary vitamins in full dosage. 

13. ETHYLDICHLORARSINE (ED) 

A. Properties. —Ethyldichlorarsine is a colorless or brown liquid which is 
more volatile than lewisite and possesses a faint fruit odor. 

B. Pathology. —The lesions are the same as those caused by lewisite. (See 
par. 12 B, C, D and E, pages 25 to 29.) 

C. Symptoms. —Low concentrations of vapor produce no symptoms for the 
first minute. Stinging pain in the nose and a burning sensation in the throat, 
nausea and vomiting then begin. Even though the gas mask is put on at once, 
symptoms may increase for several minutes. High concentrations are instantly 
so irritating to the eyes and respiratory tract that they compel wearing of the 
gas mask. A stinging and burning sensation is felt on the skin within a minute 
or two. In very hot weather this may progress to redness in ten minutes, and 
to shallow blistering in a few hours. Pain persists only about 24 hours, and the 
blisters crust over in a few days and heal rapidly. Liquid ethyldichlorarsine, 
like lewisite, is immediately painful on the skin and causes severe blistering. 
It produces eye injuries similar to, but less severe, than those due to lewisite. 

D. Diagnosis. —The following factors should be considered in making the 
diagnosis: 

(1) History of exposure. 

(2) Fruity odor of skin and clothing. 

(3) Intense sternutatory irritant, and early vesicant effect. 


29 


# 


E. Decontamination. —Decontaminating procedures are identical with those 
for lewisite. (See par. 12 B (2) and (3), page 25; par. 12 C (4), (5) and 
(6), page 27.) 

F. Treatment. —Treatment of mild respiratory tract irritation is the same as 
that for DM. (See par. 18 D, page 36.) After decontamination, eye and skin 
lesions are treated as those due to mustard. (See par. 10 B (4) and (5), 
pages 11 and 12; par. 10 C (6), (7), (8) and (9), pages 18 and 19.) 
Ointment BAL may be used in the early stages of skin erythema due to ethyl¬ 
dichlorarsine, or after severe exposure to prevent or treat systemic or respiratory 
tract injury. 

G. Prognosis. —Respiratory tract irritation from low vapor concentrations 
subsides within an hour. Skin burns, in general, heal more rapidly than similar 
mustard burns. Liquid ethyldichlorarsine contamination in the eye causes 
serious injury, possibly blindness, unless Ointment BAL is promptly adminis¬ 
tered. (See par. 12 B (2) and (3), pages 25 and 26.) 

14. PHENYLDICHLOR ARSINE (PD) 

A. Properties. —This agent, a clear viscid liquid, is less volatile than lewisite 
or ethyldichlorarsine. It is readily hydrolyzed in water. 

B. Action. —Phenyldichlorarsine when inhaled is a strong sternutator and 
lung-irritant. Eye injury produced is similar to that caused by lewisite. (See 
par. 12 B (1), page 25.) On the skin the vapor or liquid is only slightly 
less vesicant than mustard or lewisite. If absorbed, phenvldichlorarsine may 
produce systemic poisoning. 

C. Pathology. —The lesions and the systemic effects oroduced by phenyldi¬ 
chlorarsine are essentially those of lewisite. 

D. Symptoms. —Irritation of the eyes, nose and throat is prominent. Symp¬ 
toms referable to the skin and lungs are like those produced by lewisite. (See 
par. 12 C (1), page 26; par. 12 D (1), page 28.) 

E. Treatment. —Treatment in general is the same as that described for lew¬ 
isite. (See par. 12 B, page 25; par. 12 C, page 27; par. 12 D, page 28; par. 
12 E, page 29.) 


15. MIXED BLISTER GASES 

A. General .—Arsenical vesicants, such as lewisite (L) or phenyldichlorar¬ 
sine (PD) mixed with mustards may be encountered as Chemical Warfare 
Agents. Such mixtures do not produce more severe lesions than either a^ent 
alone, but they tend to confuse and make diagnosis difficult. 

B. Decontamination. —(1) Eyes. —If the exposure causes severe eye pain 
and blepharospasm, it should be assumed that an arsenical blister gas is 
present, and the first-aid measures for lewisite applied at once. (See par. 12 B 


30 


(2), page 25.) If the contamination is painless, immediate irrigation with 
water from the canteen or other uncontaminated source is employed. (See 
par. 10 B (2), page 11.) 

(2) Skin .— If stinging and burning are felt immediately, it will be assumed 
that an arsenical is present. Any excess of the liquid mixture is blotted from 
the skin at once. Ointment protective S-461 or S-330 is then applied as de¬ 
scribed under mustard. (See par. 10 C (4), page 17.) The ointment is 
thoroughly removed and Ointment BAL is rubbed on as for lewisite. (See 
par. 12 C (5), page 27.) This should be removed immediately and ap¬ 
plied again. 

C. Treatment .— (1) Eyes. —Definitive treatment of eye injuries due to a 
mixture is like that for mustard injury of the eye. (See par. 10 B (4) and 
(5), pages 11 and 12.) 

(2) Skin .— Definitive treatment of skin lesions produced by mixtures is 
like that described for lewisite burns. (See par. 12 C (8), (9), (10) and 
(11), page 28.) 


31 





- 

. 

















. 



















- 





























. 








































SECTION IV 
LACR1MATORS 


16. CHLORACETOPHENONE (CN), CHLORACETOPHENONE 
SOLUTION (CNS), CHLORACETOPHENONE TRAINING 
SOLUTION (CNB) AND BROMBENZYL CYANIDE (BBC) 

A. Symptoms .—General symptoms produced by the lacrimators include 
lacrimation, photophobia, and blepharospasm, some irritation of the nose and 
of the freshly shaven face. In hot weather moist skin will be irritated or even 
burned with blister formation. In addition, chloracetophenone solutions CNS 
and CNB may cause some mild papulovesicular dermatitis, especially in warm 
weather, and occasional vomiting. Lacrimator casualties ordinarily do not re¬ 
quire medical attention. 

B. Treatment. —(1) First-Aid. —a. Eyes .—Lacrimators produce a marked 
but self-limited irritation of the conjunctiva. When liquid lacrimators are 
splashed into the eye, the action is corrosive and resembles the burns of a 
strong acid. The instillation into the eyes of a solution of sodium sulfite (Y 4 
percent in saline), if available, dissolves and neutralizes the irritating agent. 
Eye pain may be treated by instilling Ointment Butyn Ophthalmic or eye drops 
of Solution Anesthetic. Local anesthetic should not be used unless necessary 
and then not oftener than once every 6 hours. The further treatment is 
symptomatic as for any other burns of the eye. 

b. Skin .—For skin burns caused by the lacrimators a 4 percent solution of 
sodium sulfite in 50 percent alcohol is advised. This must not be used in 
the eyes. The further treatment is the same as for other burns. (See par, 
38, page 49.) 


33 









- 























































' 

> 































































































SECTION V 

VOMITING GASES (NOSE GASES, IRRITANT SMOKES, 

STERNUTATORS ) 

17. DIPHENYLAMINECHLOR ARSINE (DM, ADAMSITE), 
DIPHENYLCHLOR ARSINE (DA), AND DIPHENYLCY AN AR¬ 
SINE (DC) 

A. General .—These agents are crystalline solids which are dispersed by heat 
as fine particulate smokes. DM smoke is canary yellow near the point of 
emission while those of DA and DC are white; all are colorless when diluted 
with air. Low concentrations are effective and suggest the odor of burning 
fireworks. 

B. These agents produce strong pepper-like irritation in the respiratory 
tract, most pronounced in the trachea and large bronchi. The onset of symp¬ 
toms may be delayed for several minutes, especially with DM, and effective 
exposure therefore may occur before the presence of the smoke is suspected. 
If the gas mask is then put on, symptoms will increase for several minutes, in 
spite of adequate protection. The casualty may believe his mask ineffective, 
remove it, and be further exposed. This is disastrous if the smoke is immedi¬ 
ately followed by a lethal gas. 

C. The gas mask offers adequate protection against these agents. 

18. DIPHENYLAMINECHLORARSINE (DM) (ADAMSITE) 

A. Pathology .—DM produces local inflammation of the nose and nasal acces¬ 
sory sinuses, throat and eyes. 

B. Symptoms .—These consist of pain and a sense of fullness in the nose and 
sinuses accompanied by a severe headache, intense burning in the throat, and 
tightness and pain in the chest. Irritation of the eyes and lacrimation are 
produced. Sneezing is violent and persistent, and coughing is uncontrollable. 
The nasal secretion is greatly increased, and quantities of ropy saliva flow from 
the mouth. Nausea and vomiting are prominent. Mental depression may 
be so marked that the individual will need to be restrained to prevent self- 
injury. 

C. Diagnosis .—This is made from the history of exposure, and the relatively 
rapid spontaneous improvement which occurs despite the original unfavorable 
appearance and condition of the individual. 


33 


* 


D. Treatment .—The mask must be worn in spite of nausea and salivation, 
but it may be lifted from the face during actual vomiting. Frequent inhalations 
of chloroform administered early, give relief; aspirin may be given to relieve 
the headache and general discomfort. Few cases should reach the medical 
service for treatment since recovery is prompt. Personnel should carry out 
their battle mission in spite of sternutators. 

E. Prognosis .—Ordinarily all symptoms disappear in approximately 1 or 2 
hours. No permanent injury occurs even in severely affected individuals. 

19. DIPHENYLCHLORARSINE (DA) AND DIPHENYLCYANAR- 
SINE (DC) 

A. The pathology, symptoms, diagnosis, treatment and prognosis are similar 
to those of diphenylaminechlorarsine (DM). (See par. 18, page 35.) 


36 


SECTION VI 

SCREENING SMOKES 


20. GENERAL 

The most important of these agents are HC mixture (HC), sulfur trioxide- 
chlorsulfonic acid (FS), and titanium tetrachloride (FAT). These smokes are 
not toxic in the usual tactical concentrations, but may be dangerous in the 
heavy concentrations formed at the immediate site of dispersion, or within 
closed spaces where accidental discharge might occur. 

21. WHITE PHOSPHORUS (WP) (See par. 28, page 39.) 

22. TITANIUM TETRACHLORIDE (FM) 

A. Pathology. —The liquid produces acid burns. 

B. Symptoms. —Smoke generated by liquid FM is unpleasant to breathe as 
it irritates the nose and throat, but it is not dangerous in field concentrations. 
Exposure of the eyes to spray will cause conjunctivitis with lacrimation and 
photophobia. Skin burns like those from acids are produced by contact with 
the liquid. 

C. Treatment. —The burned eyes or skin should be thoroughly washed with 
water and then treated like any other burn. (See par. 38, page 49.) 

D. Prognosis. —Good. 

28. SULFUR TRIOXIDE-CHLORSULEONIC ACID SOLUTION 

(FS) . ' 

A. Pathology. —Acid burns are produced by contact with the liquid. 

B. Symptoms. —These are usually limited to a prickling sensation on the skin, 
but exposure to heavy concentrations may result in severe irritation of the eyes, 
skin, and respiratory tract. 

C. Treatment. —The eye is irrigated with water at once. Fluorescein will 
reveal corneal ulceration. For pain Ointment Butyn Ophthalmic or eye drops 
of Solution Anesthetic may be instilled. The eye is then covered with a light 
pad. Skin burns should be washed with water and then with sodium bicar¬ 
bonate solution. Later treatment should be that employed for other burns. 
(See par. 38, page 49.) 

D. Prognosis. —The prognosis depends on the degree of corneal ulceration. 


37 


24. HC MIXTURE (HC) 


A. Toxicity .—Field concentrations of this smoke are harmless, but dangerous 
to fatal levels may be encountered in confined, poorly ventilated spaces or near 
the point of smoke production. 

B. Pathology .—HC smoke, if inhaled in sufficiently high concentration, dam¬ 
ages the respiratory tract by the action of the contained zinc chloride. Follow¬ 
ing severe exposure a chemical pneumonia with pulmonary edema may develop, 
as in phosgene poisoning. 

C. Symptoms .—When HC is breathed in high concentrations, there is a 
feeling of suffocation and some irritation of the nose and throat with coughing 
and choking. Later, signs and symptoms of pulmonary edema may appear. 

D. Treatment .—Treatment is like that for phosgene poisoning. (See par. 
5 D, page 4.) 

E. Prognosis .—The prognosis depends on the severity of exposure and the 
extent of pulmonary damage. 


i 


38 


SECTION VII 
INCENDIARY AGENTS 


25. GENERAL 

The principal agents of this group are thermite (TH), magnesium and 
its alloys, white phosphorus (WP) and combustible oils. All generate 
tremendous heat and can inflict severe burns. Chemical fire extinguishers con¬ 
taining carbon tetrachloride (pyrene) or liberating carbon dioxide should 
not be used in confined spaces to extinguish thermite and magnesium incendiary 
bombs. When carbon tetrachloride comes in contact with flame or a highly 
heated metal, a mixture of phosgene, chlorine, carbon monoxide and hydro¬ 
chloric acid is liberated. The service gas mask does not offer protection 
against carbon monoxide. 


26. THERMITE (TH) 

Thermite incendiaries burn at a temperature of about 4330° F. and scatter 
molten iron. Frequently, explosive charges are added and make control 
hazardous. The particles of iron that lodge in the skin usually produce multiple 
small but deep burns. The particles should be cooled immediately with water 
and removed. Thereafter, the treatment is that used for other thermal burns. 
(See par. 38, page 49.) 

27. MAGNESIUM AND ITS ALLOYS 

Magnesium burns at a temperature of about 3630° F. with a scattering effect 
similar to that of thermite. Deep burns are caused by its particles, which, 
unless removed promptly, result in slow healing. Removal is usually possible 
under local anesthesia. When explosive charges have been added to the 
magnesium bomb, the fragments may be embedded deep in the tissues, causing 
localized gas formation and tissue necrosis. 

28. WHITE PHOSPHORUS (WP) 

Extensive burns may be produced by incandescent particles of white phos¬ 
phorus. The burns are usually multiple, deep and variable in size. The smoke 
is non-toxic. White phosphorus continues to burn unless deprived of oxygen. 
The burned areas should be immersed immediately in water or covered with 
a dressing soaked with water, urine or any non-irritant aqueous solution. 


39 


Immersion should be continued until a 5 percent solution of copper sulfate 
is applied as a wet dressing. Copper sulfate forms a non-inflammable coating 
of copper phosphide on the phosphorus particles. All particles should be 
removed under water, unless the copper sulfate solution has been applied. 
They may be located by their phosphorescence in the dark. Burning particles 
are recognizable by their evolution of smoke. It is well to debride the burn 
promptly, if the patient’s condition will permit, in order to remove unnoticed 
bits of phosphorus. Following the removal of the particles, the lesions are 
treated as thermal burns. (See par. 38, page 49.) Salves with an oily 
base should not be used during the first few hours since phosphorus is soluble 
in oil and might be absorbed with resultant systemic poisoning. Otherwise 
the risk of systemic effects from embedded particles is small. Copper sulfate 
is innocuous even in large burns. 

29. OIL INCENDIARIES 

Burns may be produced by flamethrowers and by oil incendiary bombs which 
may also contain phosphorus and sodium. Lung damage from heat and 
irritating gases may be a complication added to the injuries from incendiaries, 
especially in confined spaces. Pulmonary embolism by particles of coagulated 
plasma—formed by the intense heat in peripheral veins—has been reported. 
Morphine should be given guardedly to patients with pulmonary complications. 
The treatment of burns caused by oil incendiaries is like that for other heat 
burns. (See par. 38, page 49.) 


40 


SECTION VIII 

SYSTEMIC POISONS 


30. GENERAL 

Systemic poisons produce their effects after absorption into the body and 
cause little or no local injury. Hydrocyanic acid, cyanogen chloride and arsine 
are included in this group. 

31. HYDROCYANIC ACID (AC) 

A. Physical properties .—Hydrocyanic acid is a colorless, highly volatile 
liquid which boils at 26° C. Its vapor is extremely non-persistent, and has 
the odor of bitter almond. Aqueous solutions are weakly acid. 

B. Pathology .—Hydrocyanic acid acts by combination with an enzyme es¬ 
sential for oxidative processes of the tissues. The central nervous system, 
particularly the respiratory center, is especially susceptible to this interference, 
and respiratory failure is the usual cause of death. In high concentrations of 
hydrocyanic acid (10 mg. per liter or more) the amount inhaled in a few 
breaths may be sufficient to cause immediate death without anatomical changes. 
After exposure to lower concentrations, death may be delayed for hours to 
days. Small areas of hemorrhage and softening, the more pronounced the 
longer the course, may be found in the brain in fatal cases. 

C. Symptoms .—The symptoms depend upon the concentration of the gas 
and the duration of the exposure. In high concentrations there is increased 
depth of respiration within a few seconds; violent convulsions after 20 to 
30 seconds; cessation of regular respiration in 1 minute; occasional shallow 
gasps; and finally, cessation of heart action several minutes after initial ex¬ 
posure. Following moderate exposures, vertigo, nausea and headache appear 
very early and are followed by coma and convulsions. These may persist for 
hours or days and be followed by death or recovery. If the patient recovers, 
after prolonged symptoms there may be evidence of damage to the central 
nervous system such as irrationality, altered reflexes, and unsteady gait, which 
may persist for months or longer. Mild exposure may produce headache, 
vertigo and nausea, but recovery is complete. 

D. Diagnosis .—The diagnosis may be made from the history, the odor and 
the rapid onset of symptoms. 

E. Treatment .—Under combat conditions, treatment may be difficult. When 
hydrocyanic acid is detected, the gas mask must be adjusted instantly and 


41 


the breath held as far as is possible while so doing. If one is capable of 
doing this quickly, the hydrocyanic acid already absorbed usually will be 
detoxified. If incapacitated, emergency treatment must be given instantly 
by the nearest individual. The gas mask must be applied and an ampoule of 
amyl nitrite crushed and inserted quickly under the facepiece. The patient 
should inhale the amyl nitrite for 4 to 5 minutes when another ampoule may 
be given. If the patient is conscious, he will be faint and dyspneic from 
this therapy, and may attempt to remove his mask. Artificial respiration is 
given if breathing has ceased. Where available, sodium nitrite and sodium 
thiosulfate should be administered intravenously. Sodium nitrite (10 c.c. 
doses of 1 percent solution) should be injected slowly to a total of 50 cubic 
centimeters. If necessary, epinephrine should be employed to counteract 
excessive fall of blood pressure. Between the nitrite injections 20 cubic 
centimeters of 5 percent sodium thiosulfate should be given intravenously and 
continued, if necessary, to a total of 500 cubic centimeters. Should the patient 
become greatly cyanosed as a result of methemoglobin formation, blood trans¬ 
fusions may be given. In general, treatment should be continued as long as 
there is the slightest sign of cardiac activity. 

32. CYANOGEN CHLORIDE (CC) 

A. Properties .—Cyanogen chloride is a colorless liquid which boils at 15° C. 
yielding a volatile irritant vapor. Although only slightly soluble in water, it 
dissolves readily in organic solvents. Very low concentrations (0.0025 mg. 
per liter) are sufficient to produce lacrimation. Its lethal concentration for 
10 minutes’ exposure is 0.40 mg. per liter. 

B. Pathology .—The acute toxicity of cyanogen chloride is similar to that 
of hydrocyanic acid. The respiratory center is at first stimulated and then 
rapidly paralyzed. Cyanogen chloride, like chlorine, also attacks the respiratory 
tract resulting in mild inflammatory changes in the bronchioles, and congestion 
and edema of the lungs. The edema may form more rapidly than in phosgene 
poisoning. Rarely, bacterial bronchopneumonia may complicate the original 
chemical injury. 

C. Symptoms. —The signs and symptoms combine those produced by hydro¬ 
cyanic acid and chlorine. Following exposure there is immediately intense 
irritation of the nose, throat and eyes with coughing, choking, tightness in the 
chest and lacrimation. Simultaneously the exposed person becomes dizzy and 
increasingly dyspneic. Respiration fails rapidly followed by unconsciousness 
and death within a few minutes. Convulsions, retching, ana involuntary urina¬ 
tion and defecation may occur. If these effects, due to the CN ion, are not 
fatal, the signs and symptoms of pulmonary edema may develop. There may¬ 
be persistent cough with much frothy sputum, rales in the chest, severe dyspnea 


42 


and marked cyanosis. As in phosgene or chlorine poisoning, a shock-like state 
may develop. 

D. Prevention .—The gas mask protects for a limited period. On detection, 
instantly hold the breath, apply mask and exhale. 

E. Treatment .—The treatment is that outlined for both hydrocyanic acid and 
lor chlorine poisoning. (See par. 31 E page 41; par. 7, page 6.) The 
preliminary signs and symptoms determine therapy. Artificial respiration must 
be given in cyanogen chloride poisoning if breathing has ceased. 

F. Prognosis .—If death does not follow promptly from the action of the 
CN ion, the effects of chlorine on the respiratory tract must be considered. 
(See par. 7, page 6.) 


33. ARSINE (SA) 

A. Properties .—Arsine is a colorless, odorless gas, but when impure, it may 
have a garlic-like odor in high concentrations. 

B. Pathology .—The gas is absorbed from the respiratory tract into the blood 
and gives rise to intravascular hemolysis. This results in anemia, hemoglo- 
binemia and hemoglobinuria. Through the action of circulating arsine and 
its oxidation products, there is serious disturbance of the tissue metabolism of 
kidney and liver. The kidneys show marked tubular change and numerous 
hemoglobin-albumin casts. Anatomical changes in the liver are less con¬ 
stant, but hepatitis and focal necrosis may be present. Jaundice is due to 
hemolysis or to liver damage or both. Death results from renal or hepatic 
failure, anemia, or a combination of these. 

C. Treatment .—Therapy consists of bed rest, whole blood transfusions, 
oxygen, mild diuretics and parenteral glucose. Specific therapy for arsine 
poisoning is still in an experimental stage. 


43 






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SECTION IX 

INCIDENTAL GASES 


34. GENERAL 

A. This group includes carbon monoxide, ammonia, and hydrogen sulfide. 
These may be encountered in dangerous concentrations in confined or poorly 
ventilated spaces. 

B. Protection against incidental gases. —The service mask and collective pro¬ 
tectors are not efficient against carbon monoxide, ammonia or hydrogen sulfide. 
A special type of canister is required for such protection. 

» 

35. CARBON MONOXIDE 

A. Physical properties. —Carbon monoxide is a colorless, odorless gas, which 
is lighter than air, into which it diffuses rapidly. 

B. Occurrence in military operations. —Carbon monoxide is formed by gun 
blasts, bursting shells, internal combustion engine exhaust, and by fires in 
confined spaces in ships. Dangerous concentrations are apt to occur in con¬ 
fined spaces such as poorly ventilated engine rooms, gun turrets or emplace¬ 
ments, hangar decks of aircraft carriers, tank landing craft, garages and in 
mining operations. 

C. Pathology. —Asphyxiation is produced by the inactivation of hemoglobin 
through combination with carbon monoxide. The resultant anoxia produces 
nervous system pathology. Post mortem examinations reveal little beyond the 
characteristic cherry-red color of the blood and hemorrhages in the brain. 
The dissociation of carbon monoxide from hemoglobin may be hastened by 
oxygen with or without added carbon dioxide. 

D. Symptoms. —Carbon monoxide is very insidious in its action and poison¬ 
ing may occur without appreciable initial signs. Usually, however, symptoms 
progress from throbbing headache, vertigo, yawning and poor visual acuity to 
the development of cherry-red appearance of the skin and mucous membranes, 
weakness and coma, subnormal temperature, feeble pulse and perhaps death. 

E. Diagnosis. —The diagnosis is made from the circumstances of exposure 
and the appearance of cherry-red cyanosis. 

F. Protection. —Adequate ventilation should be provided for all inclosed 
spaces where carbon monoxide may be produced. The safety of the air in 
the space may be tested by means of a standard carbon monoxide indicator. 


45 




G. Treatment. —Remove to pure air, give oxygen or oxygen-carbon dioxide 
mixture and artificial respiration if necessary. Rest, blankets, and warm drinks 
are also indicated. Blood transfusions are valuable in desperate cases. 

H. Prognosis. —The longer the period of coma the less the chance for 
recovery. The majority of mildly exposed individuals recover with early 
treatment. Tachycardia and dyspnea may continue for months, and there 
may be central nervous system disturbances ranging from simple neuritis to 
mental deterioration. 


36. AMMONIA 

A. Physical properties. —Ammonia is a colorless gas which is soluble in 
water and has a pungent, characteristic odor. 

B. Occurrence in military operations. —This gas has not been used in war¬ 
fare but may be encountered in bombings involving refrigeration plants, in 
industrial accidents and in holds of ships as a product of decomposing material. 

C. Pathology. —Exposure to high concentrations of ammonia produces 
prompt and violent irritation of the eyes and respiratory tract. There may be 
spasm and edema of the glottis or even necrosis of the laryngeal mucous mem¬ 
branes. Pulmonary edema may develop as in phosgene poisoning and may be 
complicated by bronchopneumonia. 

D. Symptoms. —Exposure to high concentrations produces violent, burning 
pain in the eyes and nose, lacrimation and sneezing, pain in the chest, cough, 
spasm of the glottis, and pulmonary edema. Often there is temporary reflex 
cessation of respiration, which with the spasm and edema may cause asphyxia. 
Concentrations of 0.1 per cent are intolerable to man. Liquid ammonia is 
vesicant. 

E. Treatment. —First-aid treatment consists of prompt removal to pure air, 
and artificial respiration. Inhalation of the fumes of weak acetic acid or 
vinegar may be of some benefit. Later measures are directed toward the pre¬ 
vention of pulmonary edema and the treatment of bronchitis and pneumonia. 
(See par. 5 D, page 4.) 

F. Prognosis. —The mortality is high following severe exposure; with lower 
concentrations, recovery is usually rapid although bronchitis may persist. 

37. HYDROGEN SULFIDE 

A. This colorless gas in low concentration has the odor of rotten eggs. 
In high concentrations it may dull the sense of smell and be difficult to 
recognize. Hydrogen sulfide, a systemic poison, is nearly as toxic as hydrocyanic 
acid. It is produced during the decomposition of sulfur-containing com¬ 
pounds in sewers, waste coal bins or stacks, holds of ships and waterfront 
excavations. 


46 


B. Pathology .—Hydrogen sulfide produces inflammation of the eyes, nose 
and throat, and in high concentrations paralyzes the respiratory center or 
causes pulmonary edema. 

C. Symptoms .—At first there is irritation of the eyes, nose and throat. 
Panting respirations and loss of consciousness follow quickly. Convulsions 
often occur as respiration ceases. If the exposure isi not sufficiently high to be 
rapidly fatal, pulmonary edema may develop. 

D. Treatment .—As heart action continues after respiration has ceased, imme¬ 
diate first-aid may be life-saving. This consists of: (1) removal of the patient 
from the contaminated atmosphere at once or adjusting his mask immediately, 
(2) artificial respiration, and (3) inhalations, if possible, of oxygen-carbon 
dioxide mixtures, or oxygen alone. The treatment of pulmonary edema de¬ 
veloping later is the same as that caused by phosgene. (See par. 5 D, page 4.) 

E. Prognosis .—Mortality from severe exposure is high. When there are 
symptoms of lung damage, the prognosis is like that in phosgene poisoning. 
(See par. 5 F, page 5.) 


47 


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SECTION X 

38. THE TREATMENT OE THERMAL BURNS 


A. Primary Objectives of Treatment. —(1) To protect the burned area, 
which is an open wound, from further contamination. 

(2) To prevent and combat shock as promptly as possible by plasma or 
albumin transfusion. 

(3) To relieve pain. 

(4) To minimize fluid loss. 

(5) To maintain optimum healing conditions by adequate protein and 

vitamin intake. x 

(6) To prevent contracture and excessive scarring by proper splinting and 
early skin grafting. 

B. First-Aid Treatment .—(1) Asepsis.- —A burn is a sterile wound; there¬ 
fore, all infection will be introduced from the outside. In the primary treat¬ 
ment of burns, it is essential that the burned area be protected from contact 
with bacteria. Contamination of the burned surfaces by organisms from the 
attendant, especially from his nose and throat, is responsible for most of the 
more serious infections which subsequently develop. Therefore, to minimize 
contamination from this source, the medical officer and assistants should be 
masked, if practicable; otherwise, mouths must be kept closed as far as 
possible. 

(2) Morphine. —Pain should be relieved by adequate doses of morphine. 
Pain resulting from an extensive burn can ordinarily be relieved by a dose 
of grain (0.030 grams) of morphine. In the presence of circulatory failure, 
there may be a delay in absorption of morphine administered subcutaneously, 
the full effect not being manifest before normal circulatory dynamics are re¬ 
stored. Therefore, caution must be exercised to control the dosage intervals, 
avoiding a cumulative effect which may result in severe morphine intoxication. 
In the presence of pronounced anoxia, large doses of morphine are dangerous, 
and under such circumstances the dose should not exceed V 4 grain (0.015 
grams). Syrettes of morphine, l/ 2 grain, are available in the first-aid pouch. 

(3) Chemotherapy. —Administer 4 grams (60 grains) of sulfadiazine by 
mouth. This is contained in the first-aid pouch. 

(4) Prophylaxis against tetanus and gas bacillus. —a. Injection. All per¬ 
sonnel with burns of the second and third degree shall be given an emergency 
injection of 0.5 (]/ 2 ) c.c. of tetanus toxoid injected intramuscularly, providing 


49 


they have received initial immunization. The prophylactic dose of gas bacillus 
antitoxin may be given at the discretion of the medical officer. 

(5) Shock therapy. —Administer plasma promptly, if available, or the 
equivalent number of units of human serum albumin, as this is an important 
element in the treatment of shock. When albumin or plasma are not imme¬ 
diately available, water should be given by mouth. 

(6) Burned area. —Do not use tannic acid or other escharotics in treatment. 
Remove rings from fingers of burned hands. Irrespective of its location, cover 
the burned surface with a liberal amount of sterile petrolatum. The burn 
should then be covered with one or two layers of sterile fine mesh gauze (44 
mesh gauze bandage is satisfactory). Place over this a smooth thick layer of 
sterile gauze dressing (large or small first-aid dressings are especially suitable 
for this purpose). Finally, a gauze or muslin bandage should be firmly applied 
over the dressing. When an extremity is involved, a splint is advised as a 
final step in the dressing. 

C. Definitive Treatment When Patient Arrives Where Hospital Facilities 
Exist. —(1) Combat shock by adequate and prompt plasma or human serum 
albumin administration. In the presence of extensive burns, quantities of 
plasma up to 12 units may be required in the first twenty-four hours. Plasma 
must be given rapidly to the patient in critical condition, if possible, not being 
allowed to flow dropty drop. Syringe injection may be used. After hemocon- 
centration has been corrected by plasma and fluids, transfusion of fresh whole 
blood, if available, should be given to combat the rapidly developing severe 
anemia which follows extensive burns; when anemia exists, whole blood 
transfusion is particularly indicated as a preliminary to skin grafting. 

(2) Parenteral fluid replacement other than that attained by means of 
plasma or whole blood transfusions should be accomplished by means of 5 
per cent glucose in sterile distilled water. The intravenous administration of 
sodium chloride solution should be reserved for those burn cases in which 
mineral depletion occurs, such as that resulting from persistent vomiting. 

(3) Minimize pain by adequate doses of morphine. 

(4) Treat the burned area as an open wound, using standard operating 
room technic with patient and attendants fully masked and gowned. 

a. Cleansing. —In cases in which the burned surface appears clean, no 
further preparation should be done. It should be reserved for gross soiling. 
If the burned area is heavily covered with fuel oil, the excess may be removed 
by gently swabbing the area with a suitable detergent, sterile lard or liquid 
petrolatum. Cleanse separately and carefully the surrounding skin with white 
soap and water. Cleansing must be done with a minimum of trauma. Do 
not use brushes in the cleansing of the burn, and avoid applying tincture of 
green soap. 


50 


b. Debridement. Loose shreds of epidermis should be carefully removed 
'ttith sterile forceps and scissors, and saved for bacteriologic study if feasible. 
Small blisters should not be disturbed, but larger ones may be punctured with¬ 
out the removal of the epidermis. Evidence of irreparable damage to deeper 
layers of skin may not be apparent for several days, and excision in such cases 
should not be done until it is certain that the tissue is dead. The resulting 
wound should be handled as any other open surgical wound, primary grafting 
of the skin being carried out as soon as conditions permit. Inhalation anesthesia 
should be avoided if possible, but intravenous anesthesia may be utilized for 
painful surgical procedures or dressings. Local anesthesia is contraindicated. 

c. Dressing of the burned area. —Tannic acid and all other escharotics will 
not be employed in the treatment of burns. Cover the burned area with 
sterile petrolatum. Strips of a line mesh sterile gauze (44 mesh gauze 
bandage is satisfactory) should be applied. Over this should be added a 
smooth, thick layer of sterile dressing; this may consist of gauze, absorbent 
cotton, cotton waste, or cellulose. The dressings should be held in place by 
an evenly and firmly applied bandage; stockinette or some form of elastic 
bandage is more effective than the ordinary roller bandage. Firm pressure is 
especially important in the case of burns of the hands and face. All dressings 
should extend well beyond the burned area, and in cases involving the ex¬ 
tremities, the dressing should start near the tip of the digits, separating them 
one from another. Uninvolved tips are left exposed to check for circulation. 
'The principle of infrequent dressings in the treatment of burns is especially 
desirable. For this reason, unless complications develop, the dressing should 
not be disturbed for from ten days to two weeks. Immobilization of the part 
by splinting should be effected when possible. 

(5) Chemotherapy .—In all cases with moderate to severe burns, prophy¬ 
lactic chemotherapy should be continued. Sulfadiazine, subsequent to the 
initial first-aid dose, should be given only under the direction of the medical 
officer. While sulfadiazine is the drug of choice, sulfathiazole or sulfanilamide 
may be substituted. It is emphasized that although sulfonamide therapy may 
prevent infection, caution must be exercised in administering such treatment 
in burn cases. The extensive fluid loss so common in these cases and possible 
kidney damage increase the danger of renal complications from sulfonamide 
therapy. Maintenance doses of sulfadiazine should be given in 0.5 grams 
( 7 I /2 grains) doses every four hours until such time as an adequate kidney 
function, a daily urinary output of at least 1500 c.c. (U /2 quarts) can be 
demonstrated, under which circumstances the dosage may be increased to 1 gram 
(15 grains) every four hours. It is recommended that 2 grams (30 grains) 
of sodium bicarbonate be administered every four hours to keep the urine 
alkaline. In the event of persistent infection despite sulfonamide therapy and 
in the event of sensitivity or of kidney intolerance, discontinue the drug. 


51 


Penicillin should then be administered in dosages of 15,000 to 20,000 units 
intramuscularly every three hours or by continuous intravenous drip in a 
concentration of 20 units per cubic centimeter of normal saline or 5 per cent 
glucose. 

(6) Skirt grajting. —One of the most important factors in preventing con¬ 
tractures and in obtaining an optimum functional and good cosmetic result 
in burns is early epithelization. For this reason skin grafting of granulating 
surfaces should always be done as soon as practicable. At the end of 10 
days or sooner, areas of part thickness loss, that is, second degree burns, should 
be largely healed. Areas of whole thickness loss, that is, third degree burns, 
are prepared for grafting by excision of the dead tissue. If suppuration is 
present, wet dressings are advisable and the local use of compresses wet with 
penicillin solution, concentration of 250 units per cubic centimeter of normal 
saline, may be helpful in combating the local infection. Skin grafting at the 
earliest opportunity is mandatory if the whole thickness of the skin was de¬ 
stroyed. Transfusion of fresh whole blood is required to combat the rapidly 
developing severe anemia complicating severe burns. When such anemia 
occurs, whole blood transfusion is particularly indicated as a preliminary to 
skin grafting. In addition, the depleted serum protein must be restored prior 
to such surgery and maintained thereafter for effective results. This is accom¬ 
plished by the judicious use of whole blood, plasma and adequate oral intake 
of protein. Where available, amino acid preparations are valuable protein 
sources which may be administered orally or parenterally to correct the grave 
protein deficiency in these cases. 


52 


\ 


SECTION XI 

39. THE CARE OF CONTAMINATED CLOTHING AND 
EQUIPMENT AT MEDICAL INSTALLATIONS 


A. Introduction. —(1) In the event of gas warfare, due care must be exer¬ 
cised at medical installations to prevent injury to patients and medical attend¬ 
ants from clothing, blankets, or other equipment, which has become contami¬ 
nated with blister gases. Proper steps must also be taken to obtain timely 
replacement of items made unusable by contamination, and to insure the 
salvage and decontamination of such equipment. For detailed instructions 
refer to Manual F.T.P. 222, "Chemical Warfare Defense Instructions" United 
States Fleet. 

• B. Removal of Contaminated Clothing and Equipment. —(1) Clothing and 
equipment contaminated with a blister gas should be removed from the casualty 
at the earliest practicable moment, with due regard for the general condition 
of the patient. 

C. Disposition of Contaminated Clothing and Blankets. —(1) An area out 
of doors should be designated as a clothing dump, and contaminated blankets 
and clothing (except impermeable aprons and rubber gloves) should be trans¬ 
ferred to this dump as conditions permit. At shore establishments the dump 
should be at a safe distance from the medical installation, preferably at least 
100 yards, down-wind. 

(2) The dump should be clearly marked "Danger, Gas." 

(3) Gas casualties should not be admitted to a hospital, sick bay, dressing 
station or other enclosed spaces unless clothing or blankets known to be con¬ 
taminated with blister gas have been removed and the patient decontaminated. 
To do so may result in severe skin burns by contact with the blister gas and 
in burns of the eyes and respiratory tract from vapors which accumulate in 
confined spaces. Provision should be made for well ventilated posts where 
decontamination can be accomplished without breaking the gas-tight integrity 
of the ship or subjecting the shore installation to contamination. 

D. Notification of Chemical Warfare Officer. —(1) The Medical Officer 
should notify the Chemical Warfare Officer advising him of the existence of 
the dump of contaminated clothing and blankets, its exact location, and ap¬ 
proximate size. 

E. The Apron, Protective Impermeable. —(1) The apron, protective, im¬ 
permeable is intended for use by personnel of the Medical Department while 
treating and handling blister gas contaminated casualties. The apron is always 


5 5 


worn in conjunction with complete permeable protective clothing, and im¬ 
permeable protective rubber gloves. The gas mask is also necessary as a part 
of the complete protective outfit. « 

(2) Litter bearers moving into dangerously contaminated areas should don 
the complete outfit described above before entering such areas. Aid station 
attendants and others should don the complete outfit prior to handling or treat¬ 
ing contaminated patients, and the apron should not be removed until the 
danger of contamination has been removed. If treatment of patients is 
hampered by the use of the impermeable gloves, such gloves may be re¬ 
moved with comparative safety after removal of all of the patient’s heavily 
contaminated clothing, and the treatment continued wearing protective cotton 
gloves. Contaminated aprons may be worn with safety for many hours in 
conjunction with permeable protective clothing. However, aprons should be 
decontaminated after each day of wear, as prolonged contact with the liquid 
blister gases may have a deleterious effect on the coated fabric. The 1 complete 
outfit should also be worn while decontaminating litters, ambulances and 
other equipment which may have been contaminated in transporting casualties. 

(3) In removing the apron care should be exercised so that contaminated 
surfaces of the apron are not permitted to come into contact with the clothing 
of the wearer or other individuals. Decontamination procedure should be 
applied as soon as practicable to contaminated articles of clothing and equip¬ 
ment. 


SECTION XII 

40. DISINFECTION OF GAS MASKS 


A. Whenever masks are stored, exchanged or used by more than one indi¬ 
vidual for training purposes, or when the wearer has been suffering from a 
cold or sore throat, they should be thoroughly disinfected. 

B. The Navy has available on its supply table approved disinfectants for 
this purpose under BuMed stock No. 1-851 and No. Sl-4790. They are 
effective germicides and fungicides. Their main advantages are that they 
do not damage the gas mask and they allow wearing of the mask within 30 
minutes. Directions for their use are as follows: 

(1) Dilutions shall be made as specified on the container. 

(2) In disinfecting the mask keep the facepiece lower than the hose and 
cannister to prevent the disinfectant from running into them. Hold the 
facepiece in the hand, saturate a small piece of clean rag with the disinfectant, 
and sponge the entire surface of the facepiece, including the outer and inner 
sides of the deflector. In this operation do not turn the facepiece inside out. 
Then apply the disinfectant similarly to the outside of the outlet valve. 

(3) Squeeze a few drops of the disinfectant from the rag into the exit 
passage to the outlet valve. Press the sides of the outlet valve with the thumb 
and finger to let the disinfectant run out. Do not shake off the excess. 

(4) Also disinfect the inner surface of the diaphragm attachment on special 
type masks. Excessive wetting of the internal parts of these attachments must 
be avoided by keeping them above the general level of the area being treated. 

(5) Allow all disinfected parts to remain moist for about 15 minutes and 
then wipe out the inside of the facepiece with a clean dry rag. The mask 
should dry thoroughly in the air (usually 30 minutes) before it is returned to 
the carrier. 

C. If approved disinfectants are not available, ordinary soap and water may 
be used, providing the mask is thoroughly dried before stowage. 

D. There are objections to the use of formaldehyde, cresol, lysol, Dakin’s 
Solution, hydrogen peroxide, copper sulfate, alcohol and other disinfectants. 
Either they destroy the mask, have a low antiseptic value, persist for a long 
time necessitating many hours for airing and ventilation, or they irritate the 
skin and breathing passages. 


55 



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SECTION XIII 

41. CHEMICAL AGENT CONTAMINATION OF FOOD 


A. General. -(1) The Medical Officer is charged with the responsibility 
to pass upon the edibility of food under conditions of known or suspected 
contamination with chemical warfare agents. 

(2) Contamination of foodstuffs by chemical warfare agents may occur 
from contact with vapor, sprays or splashes of liquid, or solid chemicals. Un¬ 
protected food supplies may be so contaminated that their consumption produce 
gastrointestinal irritation or systemic poisoning. The vesicants and arsenicals 
are the most dangerous. 

(3) While decontamination may be difficult, large stores of foods must 
not be hastily condemned until available means for decontamination have 
been considered. Scarcity of supplies may at times make reclamation necessary. 
Prompt segregation of the heavily contaminated portions may prevent or mini¬ 
mize contamination of the remainder. Generally, foods not especially packed 
in protective packages constitute the major difficulty. The present method of 
packing foods used by the Bureau of Supplies and Accounts for overseas 
minimizes the dangers of contamination. With such packaging in most cases 
only decontamination of the outer packing is required. 

B. Nature of Chemical Contamination. —The vesicants and chlorpicrin are 
readily soluble in fats. They will be absorbed by foods of high fat content, 
and because of diffusion throughout the material, it may be impossible to 
remove them. Coagulation of protein by agents which are acidic or acid 
formers in high protein foods may limit diffusion of the agent. Hydrolysis 
of acid-forming gases in foods of high water content causes decomposition 
products which render the food unpalatable. Foods of low water and fat 
content will be relatively less easily contaminated by chemical agents and less 
•difficult to decontaminate. 

C. Reclamation of Contaminated Supplies. —(1) General. —The most ef¬ 
fective and practical measures for purifying food when contaminated with 
chemical agents include washing with water or 2-5 per cent sodium bicarbo¬ 
nate solution, trimming of exposed surfaces, serrating adequately, and boiling 
in water. These measures may be ineffective, if the decomposition products 
are toxic, as in the case of lewisite. In general, food exposed to low vapor 
concentrations of chemical agents can be reclaimed by these procedures. It 
is impracticable to reclaim provisions that have been heavily contaminated by 


57 


liquid droplets of vesicant agents. Unpackaged foods on which chemical 
agents can be seen with the unaided eye should be considered spoiled and 
their purification impracticable. 

(2) Lung irritants .—This group of agents offers relatively little danger 
to food products. With the exception of chlorpicrin, these decompose rapidly 
upon contact with the water in foods, to form comparatively harmless com¬ 
pounds which may alter the flavor. Decontamination can be accomplished 
by washing, supplemented, where possible, by aeration. Chlorpicrin is slightly 
soluble in water, and is soluble in fat and most organic solvents. Its removal 
from foods of low water and fat content can be accomplished by aeration. 

(3) Lacrimators and irritant s?nokes. —a. Large stocks of supplies, when 
protected by covers or packages, probably cannot be contaminated with a 
sufficient quantity of the lacrimators or irritant smokes to warrant their de¬ 
struction. However, these agents are not easily decomposed by hydrolysis 
and it would be difficult to reclaim foods heavily contaminated by them. 

b. Dry provisions contaminated by lacrimators can be decontaminated by 
aeration. 

(4) Vesicants. —a. When contaminated with liquid mustard or a liquid 
nitrogen mustard, foods of high water or fat content are unfit for consumption 
and reclamation is not practical. When foods have been exposed to vesicant 
vapor, they can be reclaimed by washing with soda solutions and rinsing with 
clear water, intensive cooking, or in the case of dry provisions, by 24-48 hours 
aeration. Lean meat can be reclaimed by boiling in water for one-half hour 
or more, or in the case of the nitrogen mustards, with a 2 per cent solution 
of baking soda. The water must be discarded after boiling. 

b. Lewisite, ethyldichlorarsine and phenyldichlorarsine readily hydrolyze to 
poisonous arsenical oxides. Foods contaminated with these agents cannot be 
reclaimed. 

(5) Screening smokes. —a. HC, FM, FS and WP smokes are non-toxic. 
They may alter the taste of foods by acids produced on contact with moisture, 
but do no damage otherwise. 

b. Liquid FM (titanium tetrachloride) can be washed from foods. Liquid 
FS (sulfur trioxide-chlorosulfonic acid solution) is highly corrosive and forms 
strong acids on contact with moisture. It may render unfit for use foods which 
cannot be washed readily. After trimming, washing, or cooking, if the food 
does not taste too acid, it is safe to use. 

c. Unburned particles of white phosphorus are poisonous and must be re¬ 
moved from foods. Fats and oils may dissolve poisonous amounts of the 
agent and should be discarded. 


58 


(6) Other agents. —Carbon monoxide, arsine, and hydrocyanic acid will 
have little effect upon food supplies. Hydrocyanic acid is water soluble and 
foods with high water content may become unfit for consumption after ex¬ 
posure to high concentrations of that agent. 

(7) Meat from gassed animals. —It may be necessary to use animals for 
food after they have been exposed to liquid splashes of chemical warfare 
agents. Economy may justify the early slaughter of exposed animals before 
the effect of such exposure is shown. If such animals are slaughtered in an 
approved manner in the preliminary stages of poisoning and all tissues ex¬ 
posed to the gas (lungs, and other local areas) are discarded; there is no 
objection to the consumption of the meat, provided the animal passes an other¬ 
wise satisfactory meat inspection. This is true even of animals poisoned by 
arsenical agents, since the edible tissue will contain amounts -of arsenic too 
small to be toxic. Organs such as the liver, brain, heart, kidney, and lungs 
will contain relatively more arsenic than the musculature, and should be dis¬ 
carded. The meat should be well cooked. 

D. Packaged and Stored Provisions. —(1) In determining; the disposition 
of packaged and stored supplies which have been contaminated, consideration 
must be given to the nature of the contaminant as well as to the type of food¬ 
stuff and the security afforded by the packaging material. Some of these 
factors are outlined as follows: 

a. Airtight bottles and sealed tins give complete protection against vapor 
and liquid. 

b. Wooden barrels, well sealed for the exclusion of air, give complete 
protection against vapor and moderate amounts of liquid. 

c. Wooden boxes, not sealed for the exclusion of air, give little protection 
against vapor or liquid. 

d. Waxed paper boxes, well sealed for the exclusion of air, give good 
protection against vapor and fair protection against liquids. 

e. Paper wrappings give poor protection against vapor and very little against 
liquid. 

f. Foil and cellophane wrappings, sealed for the exclusion of air, give good 
protection against vapor and liquid. 

g. Ordinary textiles in a single layer packaging give practically no pro¬ 
tection against vapor and liquid. 

h. Coverings of sod and earth give good protection against vapor and liquid. 

i. Open shelters give protection against liquid sprays and splashes; closed 
buildings, against both vapors and liquids. 

j. Generally, double layers greatly increase the protective efficiency of pack- 
aging materials. 


39 


E. When it is necessary to store bulk food supplies which are poorly pro¬ 
tected by packaging, measures should be instituted to make the storage space 
as gasproof as possible. The most vulnerable foods should be placed in the 
least exposed positions, keeping in mind the fact that the vapors of chemical 
warfare agents are heavier than air and tend to accumulate in low places. In 
the field, tarpaulins covering food supplies give fairly good protection against 
vapor and liquid agents. Food supplies which have become contaminated- 
should be handled only by those trained in decontamination methods and 
equipped with protective clothing and gas masks. 


60 


SECTION XIV 

42. THE DETECTION OF WATER CONTAMINATED WITH 

CHEMICAL WARFARE AGENTS 

A. General. —(1) The medical officer is charged with the responsibility 
to pass upon the potability of water. It therefore follows that the testing of 
water for the presence of chemical warfare agents falls under his cognizance. 

(2) Contamination of water supplies with chemical warfare agents has 
been encountered rarely, but in those instances the percentage of casualties 
was high. 

(3) Methods for detecting chemical agents make it possible to determine 
safe and unsafe water. The decontamination of contaminated water is dif¬ 
ficult and should be resorted to only in extreme emergency. Decontamination 
is not a function of the Medical Department but is under the cognizance of 
the group responsible for the procurement and treatment of water supplies. 

(4) The important chemical warfare agents most likely to cause casualties 
when introduced into water are the vesicants and the systemic poisons, i.e., 
cyanogen chloride and hydrogen cyanide. It is considered improbable that 
toxic concentrations of heavy metals and alkaloids will be encountered. 

B. Toxic Limits of Chemical Warfare Agents in Water. —(1) The toxic 
limit for lewisite is 20 ppm. (20 mg/1) (10 ppm. (10 mg/1) as As 2 0 3 ), 
provided the water is chlorinated by the standard procedure for bacterial 
purification and is used for not more than one week in order to avoid 
cumulative effects. Nitrogen mustards in concentrations of 10 ppm. (10 
mg/1) have produced vomiting in man but have not caused actual casualties. 
In higher concentrations they are extremely toxic. Mustard dissolves slowly 
in water but may be found floating in tiny globules, as a film on the surface 
or collected in pools on the bottom. Small droplets when fed with water to 
rats have produced perforating ulcers in the intestinal tract. The toxic limit 
for cyanogen chloride and hydrogen cyanide are 10 ppm. (10 mg/1). 

C. Reactions With Water. —(1) The three vesicants, lewisite, mustard, 
and nitrogen mustards, all react with water to form hydrochloric acid and 
the hydrolysis product corresponding to the agent. Lewisite reacts with water 
practically instantaneously, forming the hydrolysis product "lewisite oxide" 

which is toxic and somewhat vesicant. Mustard reacts with water to form the 

# 

non-toxic thiodiglycol. A solution containing 100 ppm. (100 m/1) 


61 


mustard becomes non-toxic at the end of one hour. Some types of mustard 
contain a highly odorous compound which renders the water non-palatable 
even after hydrolysis. Nitrogen mustards hydrolyze slowly to a non-toxic 
product. A solution containing 100 ppm. may remain toxic for 4 to 6 days. 
Cyanogen chloride, hydrogen cyanide, and heavy metal salts dissolve in water 
but do not react extensively with it. 

D. Detection of Chemical Warfare Agents in Water. —(1) The water 
testing, screening kit approved by the Bureau of Medicine and Surgery af¬ 
fords simple and rapid tests of raw water to detect dangerous contaminations 
by chemical warfare agents. 

(2) The kit contains equipment for testing 15 samples of water. The 
tests employ dry reagents which are furnished as tablets or pellets of proper 
size. Except for warming with the hand in some of the tests, no heat is 
required. 

(3) The kit also contains a booklet which gives specific directions for each 
test. Non-technical language is used and the reagents are referred to by 
the letters on the vials. These directions must be followed exactly. Briefly 
the tests involve the following chemical processes: 

a. Arsenicals are converted to arsines through the action of hydrogen, pro¬ 
duced by the action of sodium acid sulfate on zinc. The arsine reacts with 
a sensitized paper to produce a stain. This is sensitive to 5 ppm. 

b. The pH of the water is determined by means of nitrazine test papers. 
These papers test over a pH range from 4.5 to 7.5. 

c. Mustard is detected by means of the DB-3 reagent in pellet form; 5 ppm. 
(5 mg/1) of nitrogen mustard can be detected. Cyanogen chloride produces 
a yellow color with this reagent. 

d. The chlorine demand or chlorine uptake is determined by means of 
halazone tablets and an O-tolidine testing assembly. This test includes the 
presence of a number of less important agents not specifically tested for. 

e. If no evidence of contamination is found, odor and taste can be tried 
with safety. 

E. Directions for Use of Kit, Water Testing, Screening. —(1) Purpose .— 

a. The water testing kit is employed to screen out sources of water so contami¬ 
nated with chemical agents that they cannot be rendered potable by customary 
field treatment methods, such as chlorination in the Lyster bag. Individuals 
performing the tests must have normal color vision. 

b. Negative tests indicate water suitable for chlorination and may there¬ 
after be used. 

c. If any of the tests are positive, the water should not be used until a 
more complete analysis can be made. 

d. The main purpose of the kit is to detect contamination by chemical 
agents in raw water. It is not designed for use in the control of chlorine 


62 


treated water. Chemical reactions during water treatment invalidate-' the in¬ 
terpretations. 

F. Procedures for Tests .— (1) General. —a. Read directions thoroughly. 

b. Obtain water sample in canteen cup without excessive disturbance of 
water source. 

c. Start the arsenic test. While the arsenic test is developing, carry out the 
other tests. 

(2) A rsenic test. —a. Pour suspected water into the bottle (P) to mark 
on bottle. 

b. Place 2 tablets from vial A into the bottle. Shake to dissolve. 

c. Take a test strip from vial B by the top end. Carefully insert into the 
tube (H) bending the strip near the top so that it will remain in the upright 
tube. Touch only the top end of the strip. Keep dry. 

d. When the tablets (A) have disintegrated, add 5 tablets from Vial C to 
the contents of the bottle P. 

e. Promptly fit the test paper assembly into the bottle. 

f. If cold, warrr^ the bottle in your hands. Let react for 20 minutes. 

g. Remove the strip and note the length of the yellow to brown stain. A 
stain inch or more indicates a positive test. A stain less than inch indi¬ 
cates a negative test. 

(3) pH Test .-—Dip a strip of the nitrazine paper into the water until it 
becomes wet. Remove and compare resulting color with color chart on case 
lid. pH less than six (6) indicates possible contamination. 

(4) Mustard Test (Including Nitrogen Mustard and Cyanogen Chloride).— 

a. Rinse test tube with suspected water. 

b. Carefully fill test tube to l/ 2 i nc h depth with suspected water. 

c. Add one tablet from vial D. 

d. Shake for 3 minutes, to break up the tablet. Allow to stand for 3 
minutes. 

e. During cold weather, warm tube in hand or inside pocket for additional 
5 minutes. 

Note: Yellow color after d or e is positive test for Cyanogen Chloride. 

f. Break one tablet from vial E in half and add both halves to water being 
tested. 

g. Shake until broken up. While shaking, watch for the development of 
any color. 

h. Observe for l/ ? minute against white background. 

i. Even a slight blue or red color (mainly in curd) indicates a positive test 
for mustard or nitrogen mustard. 

j. A yellow color indicates CNCI. In heavy contamination the yellow 
color appears before step (f). 

k. White or light gray color indicates a negative test for mustards 


63 


(5) Chlorine Demand Test. —a. Fill a canteen with water to within an 
inch of the top. 

b. Add three (3) tablets from vial F, screw cap on and shake to dissolve. 
(2-5 min.) 

c. Five (5) minutes after tablets have dissolved transfer treated water from 
canteen to plastic tube with yellow band, of vial X testing set, filling the 
plastic tube to bottom of yellow band. 

d. Add one tablet from vial X, shake and note color when dissolved. 

e. A positive test is indicated by no color or color lighter than yellow band 
in plastic tube. 

f. A negative test is indicated by an orange color or color as deep as the 
yellow band. 

(6) Taste and Odor. —(a) If test F(2), arsenic; F(4), mustard; F(5), 
chlorine demand; are negative, and pH is six or above, carefully smell and 
taste a small sample of the suspected water. 

a. A positive test is indicated by: 

i. a lacrimating or chlorinous odor. 

ii. a biting and/or peppery chlorinous taste. 

iii. any taste or odor of a known war gas. 

b. Absence of all tastes or odors will indicate a negative result but not neces¬ 
sarily a safe water. A negative test is also indicated by the presence of only 
those odors and/or tastes normally characteristic of natural water. 

(7 ) Interpretations: 


Test 

CONTAMINATED 

WATER 1 

NONCONTAMINATED 

WATER 2 

Arsenic test, (F2) . 

Positive 

Negative. 

pH test, (F3) . 

pH below 6 . 

pH above 6. 

Mustard test, (F4) . 

Positive . 

Negative. 

Chlorine Demand, (F5) 

Positive . 

Negative. 

Taste and Odor, (F6) 

Positive . 

Negative. 


1 Water will be considered contaminated if one or more of the tests gives l'esults as 
indicated in this column. 

2 Water will be considered suitable, after bacWial disinfection by usual methods for 
one week if all the tests give results indicated in this column. 

G. Sensitivity and Limitations of the Tests. —(1) If the tests are carefully 
performed, the threat of serious casualties from using water contaminated with 
chemical warfare agents will be avoided. 

(2) The arsenic test will show whether any arsenic is present or not. The 
lengths of stain on the strips of test paper, produced by 5, 10 and 15 ppm. 
of arsenic or arsenic in the form of organic arsenicals are sufficiently different to 
manifest approximately how much arsenic is present. Inorganic arsenite or 


64 





















arsenate produce very long, dark stains at the above concentrations. The test 
for arsenic allows some latitude in the interpretation of the results. If the 
stain on the test is not longer than one-fourth inch, the arsenic content is not 
more than 10 ppm. as organic arsenic. This water may be used for a period 
not to exceed one week because of possible cumulative effects, provided all 
the other tests are negative and the water is thoroughly chlorinated. If the 
stain is longer than inch, the water shall not be used. 

(3) The pH test is a general screening test. A pH below 6.3 should be 
regarded with suspicion unless the character of the water source seems to 
indicate a naturally low pH. Contamination of the water by mustard, the 
nitrogen mustards or the arsenicals would lower the pH as all these chemical 
agents release hydrochloric acid in water solution. A pH above 8.5 probably 
means contamination with some basic material as potassium cyanide. 

(4) The test for mustards will detect mustard or the nitrogen mustards in 
5 ppm. Thiodiglycol will not react. Ethyl iodoacetate and Chloroacetophenone 
will also react, but these can be easily detected by their odor. Cyanogen 
chloride gives a yellow color with the mustard test and can be detected as 
low as 10 ppm. No blue color develops when the RB tablet is added. If the 
test for mustard and the nitrogen mustards is positive, the water should be 
rejected for all purposes. Water may 1 pass the test for nitrogen mustards and 
still give symptoms if consumed in large quantities. Therefore the water 
should not be used without special purification if even the faintest blue color 
develops. When the result of the test is questionable, the amount of water 
permitted per man at the first drinking should be limited to one-half pint; if 
no symptoms cf nausea or vomiting develop during the succeeding two 
hours, the water may be used freely thereafter. 

(5) The O-tolidine reaction used to detect chlorine residuals in the chlorine 
demand test is sensitive to 0.1 ppm. of chlorine. A chlorine residual does 
not mean a safe water. It has been shown that water contaminated with 
mustard or thiodiglycol may show a chlorine residual and actually still have 
a chlorine demand. An excess of 4 to 5 ppm. of chlorine above what is 
needed for the actual chlorine demand is necessary in order to have complete 
reaction between the chlorinating agent and the mustard or thiodiglycol. If 
this condition is not met, the water will show a chlorine residual as determined 
by the O-tolidine reaction when it still has a chlorine demand. Other colors 
may be obtained when using the O-tolidine reaction. If the color is blue or 
green, it means there is too much O-tolidine for the amount of chlorine present. 
A red or orange color means that too great an amount of chlorine has been 
added. A high chlorine demand means contamination with mustard, 
thiodiglycol, arsenicals or pollution by organic waste material. If the arsenic 
test is negative, the chlorine demand is a measure of contamination by mustard. 


65 


However, the water may also be contaminated with the nitrogen mustards. 
These compounds do not react in the chlorine demand test. 

(6) The tests provided by this kit are not quantitative, and therefore will 
serve as a guide for the purification of water supplies only within the limitation 
specified. 

H. Action Required if the Water Is Round Contaminated by Chemical 
Warfare Agents. — (1) Whenever positive tests are obtained with the water 
testing kit, the water will be considered contaminated and the following action 
taken: 

a. The Commanding Officer will establish the necessary safeguards to pre¬ 
vent men from drinking the contaminated water. 

b. An alternative source of uncontaminated water should be sought and, 
if found, should be employed. 

c. If a source of uncontaminated water cannot be found, consideration 
should be given to moving to a different location, or to importing purified 
water. 

d. In any event, the contaminated water should not be used by men until 
it is purified and then only after every effort has been made to obtain an un¬ 
contaminated supply. 

e. Contamination discovered in otherwise suitable water should be reported 
as promptly as possible to the Commanding Officer so that the matter can be 
brought to the attention of the officer responsible for purification. 

I. Scale for Issue of Water-Testing Kits. —As the kit is expendable, the 
individual items of its contents are not supplied for refilling. When the 
contents have become exhausted, the complete kit can be replaced through 
the usual channels of medical supply. 

J. Use of Suspected Water. —(1) Water which is only slightly contami¬ 
nated can be used for periods not to exceed 1 week after chlorination for 
bacterial pollution. 

(2) When suspected water is used, great care should be taken not to 
stir up material from the bottom as it may contain chemical agents when the 
water above does not. 

K. Procedure in Case of Heavy Contamination. —When water is too heavily 
contaminated to pass the Screen Kit test, every effort should be made to 
secure another source or to have pure water supplied. If pure water is not 
available, treat the contaminated water as outlined briefly below. Only 
trained personnel should undertake such procedures. 

L. Purification of Contaminated Water. —(1) Water must be withdrawn 
from the intermediate levels with minimum disturbance of the surface and 
no disturbance of the bottom. 


66 


(2) 1 reatment oj large volumes. 

a. The contaminated water is pumped into a canvass reservoir and a quan¬ 
titative analysis made by the responsible officer. 

b. It is then treated with activated carbon (200 mesh) in the following 
doses: 

i. For lewisite, 30 ppm. (30 mg/1.) carbon for each ppm. (mg/1.) 
lewisite. 

ii. For mustard, 30 ppm. (30 mg/1.) carbon for each ppm. (mg/1.) 
mustard. 

iii. For nitrogen mustard, 60 ppm. (60 mg/1.) carbon for each ppm. 
(mg/1.) nitrogen mustard. 

c. The carbon and water are mixed for 20 minutes to insure complete 
absorption of the agent by the carbon. 

d. 175 ppm. (175 mg/1.) of coagulant is added to the carbon-dosed water, 
together with sufficient alkali to give optimal coagulation. 

e. After thorough, gentle mixing, the water is allowed to coagulate and 
clarify by sedimentation for 30 minutes. 

f. The supernatant water is filtered through the portable water purification 
unit, at normal rate 8 —(— 10 gpm., or preferably more slowly. 

g. The filtered water must be tested quantitatively to see that it meets the 
following requirements: 

i. Mustards—not more than 2 ppm. (2 mg/1.). 

ii. Lewisite (arsenicals) not more than 20 ppm. 20 mg/1.). 

iii. pH above 5. 

iv. Chlorine demand, less than 5. 

v. No chemical odor or taste. 

(3) Treatment in Lyster Bags. 

a. When the portable water purification unit is not available, small volumes 
can be purified by using two Lyster bags. 

b. If testing equipment is available to identify the contaminating agents 
and determine their concentrations, add activated carbon in the dosages given 
in par. L (2), to the water in one Lyster bag. If the identities and concen¬ 
trations of contaminants are unknown, add 2 lbs. activated carbon. 

c. Stir for 20 minutes. 

d. Add 1 ounce of alum and sufficient alkali to give optimal coagulation. 
These chemicals should be dissolved separately in small volumes of water 
prior to their addition to the Lyster bag. 

e. After thorough, gentle mixing, allow to coagulate and clarify by sedimen¬ 
tation for 30 minutes. 

f. Siphon the supernatant water to another Lyster bag (preferably through 
a filter). 


67 


g. After testing to insure that the requirements of par. L (2) g, page 67, 
are met, the water in the second Lyster bag must be chlorinated. 

M. Chlorination of Contaminated Water .—Chlorine reacts with some of 
the chemical agents making it difficult to remove them by the activated carbon 
and alum treatment. Therefore, chlorination should be carried out only after 
filtration through the portable purification unit, and the chlorine feed-line 
must be connected to the effluent pipe from the filter. In the case of treat¬ 
ment in the Lyster bag, chlorine is added in the second Lyster bag. When 
contamination is suspected, no chlorinating compounds should be added until 
the water has been clarified. 


68 


SECTION XV 


43. MANAGEMENT AND TRANSPORT OF CHEMICAL 
WARFARE CASUALTIES IN NAVAL AND 
MARINE FORCES 

A. General. —(1) Casualties unable to apply self-aid are cared for by 
the medical services. A casualty is defined as one who is no longer able to 
carry out his military duties as a result of injury. 

(2) Non-casualties who are contaminated are charged with the respon¬ 
sibility of self-aid at the earliest possible moment consistent with battle 
conditions. 

(3) The management and transport of contaminated gas casualties whether 
wounded or otherwise will be governed primarily by military considerations. 

(4) To facilitate the management and transport of gas casualties, the medi¬ 
cal officer whether afloat or ashore shall develop a practicable and safe plan 
applicable to the command to which he is attached. This plan shall be in¬ 
corporated in the gas defense bill of that unit. 

(5) Certain improvisations may be necessary to activate such a plan. The 
basic principles of management and transport must be clearly understood and 
applied in order to make it effective. 

(6) The most difficult problems of management and transport concern 
casualties contaminated with blister gas. 

B. Principles of Management and Transport. —(1) Avoid spread of con¬ 
tamination: 

a. If gas warfare agents have been used, it must be assumed that all cas¬ 
ualties are contaminated until proved otherwise. 

b. Personnel shall take all reasonable precautions to protect themselves 
adequately while handling contaminated casualties. If blister gas is en¬ 
countered they must wear the mask, protective ointment, protective suits, pro¬ 
tective gloves, rubber overshoes and an impervious apron. In an emergency 
the individual protective cover issued to advanced base personnel may be used 
instead of the impervious apron. These items, except the mask and pro¬ 
tective cover, are contained in the gas casualty treatment case, unit No. 10, 
Med. Supply Catalog Item 14—055. 

c. Personnel handling contaminated casualties shall avoid spreading con¬ 
tamination to other personnel and to facilities not specifically designated for 
the reception of gas casualties. 

d. Contaminated personnel, casualties, clothing and equipment must be pre- 


69 


vented from gaining access to totally enclosed spaces either afloat or ashore. 
Interior contamination of the ship or of enclosed structures ashore must be 
avoided. 

e. Contaminated clothing and equipment shall be placed in tightly cov¬ 
ered containers marked for the purpose, or in designated dumps sufficiently 
far moved from the scene of activities, for decontamination or disposal as 
determined by the chemical warfare officer. 

(2) First Aid: 

a. The problem will arise frequently as to which condition requires pri¬ 
ority of first aid, the surgical condition or the gas hazard. 

b. In all instances such as severe hemorrhage or shock, the surgical con¬ 
dition takes priority of action. 

c. If the surgical condition permits delay, the casualty shall be decon¬ 
taminated on the spot, protected from further exposure and, if consistent 
with battle conditions, transported to the nearest aid station designated to 
receive gas casualties. 

C. Transport of Gas Casualties. —(1) Stretcher bearers adequately trained 
and equipped to handle gas contaminated casualties should be detailed to 
transport such cases. 

(2) The gas hazards attending the management and transport of contami¬ 
nated casualties in operations ashore may be enhanced by the distances in¬ 
volved and by the character of the terrain, foliage and weather. Afloat, the 
hazards tend to be increased by the limited topside space available for de¬ 
contamination, the provisions for gas integrity of the ship, and the small 
openings and passageways which limit transport to dressing stations. 

(3) Ashore, the hazards of transporting gas contaminated casualties by 
stretcher shall be minimized by using two stretcher covers, if available as 
follows: 

a. Stretcher Cover No. 1. 

a. This cover shall be the impervious cover issued to advanced base naval 
and Marine Corps personnel. Medical officers of advanced bases shall ar¬ 
range to draw the necessary supply of this item from the stock to be main¬ 
tained by the Bureau of Ships in these areas. If not available from this 
source it may be obtained from the casualty encountered or other personnel 
as in the case of the Marine Corps. Medical officers attached to Marine 
Corps units shall utilize the impervious protective cover carried in the gas 
mask carrier of the casualty transported, or from other personnel, as the 
Marine Corps does not maintain a reserve stock for use as stretcher covers. 
In an emergency, the poncho carried by Marine Corps personnel in combat 
areas may be utilized. 

b. For use on the stretcher the cover will be split up each side or up one 
side and across the top. 


70 


c. The use of a clean impervious cover with each casualty permits the al¬ 
ternate transport of a wounded, but clean casualty, by the same stretcher, 
since it prevents contamination from the stretcher to the casualty and vice 
versa. 

b. Stretcher Cover No. 2. 

a. This cover is an ordinary unimpregnated blanket routinely issued to 
stretcher bearers. 

c. If two stretcher covers, No. 1 and No. 2 are used the following pro¬ 
cedure should be carried out: 

a. Stretcher Cover No. 2 is laid over No. 1 and both are folded over so 
as to bring the side edges to the center. They are to be folded again and 
the ends turned in to fit the stretcher, when in the carrying position. 

b. The prepared stretcher is placed beside the casualty; first aid is ad¬ 
ministered; the covers are unfolded; the casualty is laid on No. 2 cover; the 
sides are folded over the casualty and transport begun. 

d. Transport by ambulance or other enclosed vehicle of the contaminated 
gas casualty cannot be undertaken except with grave risk of contaminating its 
interior. Casualties must be decontaminated before such transport. 

e. Upon depositing the casualty at the aid station the stretcher covers are 
to remain with the casualty. Clean covers (if available), previously folded, 
are to be laid into the stretcher for the transport of another casualty. 

(4) Afloat, the problems of transport do not warrant the use of the im¬ 
pervious protective cover. This item is not issued to naval vessels. It is 
advised that an ordinary blanket be substituted, even though it is pervious 
to vesicant liquid or vapor. This is preferred to leaving the casualty com¬ 
pletely exposed. The blanket must be subsequently handled as a contaminated 
item. 

(5) For all activities, it must be emphasized, that if the stretcher is not 
equipped to limit undue hazards, it becomes contaminated and must be 
handled as such. 

D. Aid Stations for Gas Contaminated Casualties. —(1) Aid stations shall 
be improvised with free ventilation, upwind from the gassed area and pro¬ 
tected as much as possible against drops of liquid gas from overhead struc¬ 
tures or foliage. In no event shall it be an enclosed space. 

(2) The station shall be located in a gas-free area, if possible. If a con¬ 
taminated area must be selected, proper decontamination shall be carried out. 
Afloat, this is accomplished by using the non-corrosive decontaminating agent 
RH-195 issued by the Bureau of Ships. Ashore, chloride of lime (also 
known as bleach) is satisfactory. Bleach may be spread over the area either 
as a powder or mixed with water. 

(3) The aid station shall be clearly posted for easy identification and shall 
be marked off into an unclean and a clean area, the latter being on the wind¬ 
ward side. 


71 


a. The unclean area: 

a. The unclean area should be equipped with tightly covered G. 1. cans 
or similar receptacles for reception of contaminated clothing and equipment, 
a reserve stock of protective ointment S-461 or S-330 and BAL Ointment, 
an adequate supply of water and soap for cleansing, standard first aid equip- 
ment for the care of wounded casualties and a foot box containing RH-195 
powder or bleach powder through which all personnel must walk in going 
from the unclean to the clean area in order to decontaminate foot gear. It 
is advisable also to improvise stands (sawhorse or the like) for supporting 
the stretcher and casualty above the terrain or deck. 

b. The contaminated casualty deposited in the unclean area shall receive 
first aid. All contaminated clothing, equipment, covers, blankets and valu¬ 
ables, except the gas mask, if worn, shall be placed in specified G. I. cans 
for disposal by the chemical warfare officer. The casualty is to be further 
cleansed by the removal of all gross liquid agents and by the application of 
antigas ointment and other decontaminating procedures as outlined in Manual 
NavMed, 220 "The Treatment of Casualties from Chemical Warfare Agents.” 
The casualty is then ready for transfer to the clean area in a clean stretcher 
and/or clean covers and blankets. 

b. The clean area: 

a. The clean area shall be reserved for decontaminated casualties. Before 
entering this area, the gas mask shall be removed if the atmosphere is gas- 
free. Additional first-aid measures may then be carried out, after which the 
casualty is ready for transport to a battle dressing station or to a shore medical 
facility for further specific treatment. 


SECTION XVI 


NAVY MEDICAL SUPPLY DEPOT ITEMS FOR SELF-AID AND 
DEFINITIVE TREATMENT OF CHEMICAL WARFARE 

CASUALTIES 


Stock No. 

Item 

Unit 

Quantity 


S2-1038 Kit, First Aid (Gas Casualties): 




( contents ) 



1-140 . 

AMYL NITRITE, 5 minim pearl . 

12 in box 

1 

1- . 

COPPER SULFATE SOLUTION, 10'% with 




BLUNT DRESSING FORCEPS. 

pkg 

1 

Sl-^55 

OINTMENT ANESTHETIC . 

1-07 lube 

1 

Sl-3361 . 

OINTMENT BAL 

l/^-oz tube .. 

1 

Sl-3365 . 

OINTMENT, BUTYN OPHTHALMIC, 



2'% . 

1-dr tube 

2 

S1-3 37 5 . 

OINTMENT, PROTECTIVE, S-461 

3-oz tube 

2 

S2-845 . 

COTTON PADS, 1- by 2-in 

50 in pkg .. 

1 


14-033 Field Medical No. 10 CASE, 




Treatment Chemical Casualties 




Packing: Four hard fiber suitcases, 26- 




by 13- by 9- in. Weight: Case No. 1, 43 




lb; case No. 2, 25 lb; case No. 3, 40 lb; 




case No. 4, 30 lb. Total cubic measure- 




ments: 7.6 cu ft. 




Case No. 1 



1-140 

AMYL NITRITE, 5 minim pearl 

12 in box 

8 

1-245 . 

CHLOROFORM (for anesthesia) 

14 -lb bot 

2 

1-285 . 

CUPRIC SULFATE 

2-oz bot 

4 

1-495 . 

MORPHINE TARTRATE, 0.032-gm, U/ 2 




cc tube with sterile needle 

syrette . 

5 

1-725 . 

SOAP, hard (Castile) . 

1-lb pkg 

1 

1-745 . 

SODIUM, BICARBONATE . 

1-lb ctn 

1 

1-995 . 

CODEINE SULFATE, 0.0l62-gm 

100 bot . 

1 

2-135 . 


one . 

6 




2-350 . 

COTTON, absorbent, compressed . 

1-oz pkg 

6 

2-435 . 

GAUZE, plain, compressed . 

1-oz pkg 

25 

3-766 . 

SHEARS, bandage, angular, 5 1 / 2 ' in (Lyster) 

one 

1 


73 























































Stock No. 

Item 

L'nit 

Quantity 

3-865 . 

SUITCASE, hard fiber, 24- by 12 - by 8 -in 

one . 

1 

4-110 

BOTTLE 8 -fl-oz . 

doz . 

1/12 

4-745 . 

MEDICINE DROPPER 

doz . 

a 

6-235 

SPOON table . 

one . 

1 

13-025 . 

BASIN, hand, rubber, collapsible 

one . 

1 

13-185 

STIRRER wood Yz~ by 12-in 

one 

1 

13-210 . 

TIN, i/>-gal capacity 

one . 

1 





14-280 . 

CASE, canvas, carrying 

one . 

1 





14-500 . 

SPOON, tea . 

one . 

1 

Sl-3355 .... 

OINTMENT, ANESTHETIC 

1 -oz tube . 

5 

S1-3361 

OINTMENT, BAL 

tube . 

50 

S1-3362 . 

OINTMENT, BORIC ACID 

4-oz tube ... 

10 

Sl-3365 . 

OINTMENT, BUTYN, ophthalmic 2 '% . 

1 -dr . 

12 

S1-3375 . 

OINTMENT, PROTECTIVE, S-461 

3 -oz tube 

50 

Sl-3785 .... 

SOLUTION, ANESTHETIC 

1 -oz bot 

1 

S7-300 . 

TREATMENT OF CASUALTIES FROM 




CHEMICAL AGENTS 

one . 

1 


Case No. 2 



1-140 . 

AMYL NITRITE, 5 minim pearl 

12 in box 

7 

1-245 . 

CHLOROFORM (for anesthesia) 

l/ 4 -lb bot. 

2 

1-285 . 

CUPRIC SULFATE 

2 -oz bot . 

4 

1-495 . 

MORPHINE TARTRATE, 0 . 032 -gm, li/ 2 - 




cc tube with sterile needle . 

syrette . 

5 

1-725 . 

SOAP HARD (Castile) 

Mb pkg 

1 

1-745 . 

SODIUM BICARBONATE 

1 -lb ctn . 

1 

1-980 . 

ACID, ACETYLSALICYLIC, 0.324-gm 

1,000 bot ... 

1 

1-995 . 

CODEINE SULFATE, 0 . 0162 -gm 

100 bot 

1 

2-135 . 

BATH, eye . 

one . 

6 

2-350 . 

COTTON, absorbent, compressed 

1 -oz pkg .... 

6 

2-435 . 

GAUZE, plain, compressed . 

1 -oz pkg .... 

25 

3-7 66 

SHEARS, bandage, angular 5 Y 2 in 

one . 

1 

3-865 . 

SLTTCASE, hard fiber, 24- by 12 - by 8 -in 

one 

1 

4-730 . 

MEASURE, glass, graduated, 500-cc . 

one . 

1 

4-745 . 

MEDICINE DROPPER 

doz . 

Vi 

13-025 

BASIN, hand, rubber, collapsible 

one . 

1 

13-185 . 

STIRRER, wood, Yl~ ^y 12 -in 

one . 

> 1 

13-210 . 

TIN, V 2 "gal capacity . 

one 

1 





14-280 . 

CASE, Canvas, carrying . 

one 

1 

14-500 . 

SPOON, tea . 

one 

1 

Sl-3355 

OINTMENT, ANESTHETIC 

1 -oz tube 

5 

Sl-3361 .... 

OINTMENT, BAL 

tube . 

50 

S1-3362 . 

OINTMENT, BORIC ACID 

4-oz tube . 

10 

Sl-3365 . 

OINTMENT, BUTYN, ophthalmic 2'% . 

1 -dr tube 

, 12 

S1-3375 .. . 

OINTMENT, PROTECTIVE, S-461 

3 -oz tube 

50 

S1-3 565 

POWDER, BLEACHING, HIGH TEST 




HYPO 

3 %-lb cont 

1 

Sl-3785 . 

SOLUTION, ANESTHETIC 

1 -oz bot ... 

1 


74 































































































































Stock No. 

Item 

Unit 

Quantity 


Case No. 3 



3-865 . 

SUITCASE, hard fiber, 24- by 12- by 8-in. 

one . 

1 

13-025 . 

BASIN, hand, rubber collapsible 

one 

? 

13-105 . 

GLOVES, acid, rubber 

pair 

« 

14-280 . 

CASE, canvas, carrying .... 

one 

1 

Si 3-010 . 

APRON, impermeable, surgeon’s 

one . 

7 

Si 3-500 . 

OVERSHOES, rubber .. 

pair 

8 


Case No. 4 



3-865 

SLUTCASE, hard fiber, 24- by 12- by 8-in. 

one . 

1 

14-280 . 

CASE, canvas, carrying . 

one 

1 

Si 3-700 . 

SLTT, gas-resistant, 2-piece 

one 

8 


ADDITIONAL ITEMS NOT IN UNIT 


Stock No. 

Item 

Unit 

1-150 . 

ATROPINE SULPHATE 

15-gr vial. 

1-170 . 

BISMUTH SUBCARBONATE 

1 -lb ctn. 

1-175 . 

BISMUTH SUBNITRATE . 

l/ 4 -lb boc. 

Sl-2601 . 

FLUORESCEIN SODIUM 

10 -gm bot. 

S1-1130 . 

PENICILLIN SODIUM, CRYSTALLINE 100,000 



Oxford Units . 

Ampule. 

S1-3530 . 

PLASMA Normal Human Dried . 

250 cc 

S1-3531 . 

PLASMA Normal Human Dried. 

500 cc. 

Sl-4315 . 

SODIUM BICARBONATE 0.648 gm. 

100 bot. 

S1-4316 . 

SODIUM BICARBONATE 0.648 gm. 

1,000 bot. 

Sl-3808 

SULFADIAZINE 1 gm Tables. 

24 pkg. 

S1-4341 

SULFANILAMIDE 0.324 gm Tablets. 

100 bot. 

Sl-3790 . 

SOLUTION DEXTROSE (glucose) 5 percent 



normal . 

1,000 cc. 

S1-3795 . 

SOLUTION Normal SALINE 

1,000 cc. 

Si-2092 . 

TETANUS TOXIDE Alum Precipitated 

10 -cc vial. 

Si-4790 . 

ZEPHIRAN CHLORIDE aqueous (concentrate) 

4-oz bot. 


75 

















































































SECTION XVII 


SYLLABUS OP INSTRUCTION AND TRAINING IN CHEMICAL 
WARFARE DEFENSE FOR ALL MEDICAL PERSONNEL 

(10-Hour Course) 

A. Basic Gas Defense Instruction and Training. —(1) 5-hour, 10-hour, or 
24-hour course depending upon the local command. The Chemical Warfare 
Officer of each unit or sub-unit is responsible for this training which includes 
all naval personnel (Ref. Section 12, CNO Manual FTP. 222, ''Chemical War¬ 
fare Defense”). 

B. Medical Gas Defense Instruction and Training. —(1) General. 

FIRST HOUR 

a. Introduction to problem. 

b. War gases; physiological classification of: 

i. Blister gases. 

ii. Choking gases. 

iii. Blood and nerve poisons. 

iv. Vomiting gases. 

v. Tear gases. 

c. Screening smokes. 

d. Incendiaries. 

(2) EfFects of chemical warfare agents on the body; self aid, first aid, and 
treatment relating to the eyes, the skin, the respiratory tract and systemically. 

SECOND HOUR-BLISTER GASES 

a. Mustard gas (FI). 

b. Nitrogen mustard gas (KN). 

THIRD HOUR—BLISTER GASES, CONTINUED 

a. Lewisite (L), Ethyldichlorarsine (ED), Phenyldichlorarsine (PD). 

b. Mixed blister gases (H & L, HN & L, etc.). 

FOURTH HOUR-CHOKING GASES 

a. Phosgene (CG), Diphosgene (DP), Chlorpicrin (PS), Chlorine (CL), 
Nitric Fumes. 

FIFTH HOUR—BLOOD AND NERVE-POISONS AND TEAR GASES 

a. Hydrocyanic Acid (AC), Cyanogen Chloride (CC), Arsine (SA). 

b. Chloracetophenone (CN), Chloracetophenone Solution (CNS), Chlor- 
acetophenone Training Solution (CNB), Brombenzylcyanide (BBC). 


77 


SIXTH HOUR—VOMITING GASES AND SCREENING SMOKES 

a. Adamsite (DM), Diphenylchlorarsine (DA), Diphenylcyanarsine (DC). 

b. Hexachlorethane Mixture (HC), Sulfur Trioxide (FS), Titanium 
Tetrachloride (FM), White Phosphorus (WP). 

SEVENTH HOUR 

a. Incendiaries: Thermite (TH), Magnesium (TH), Oil Incendiaries 
(IM) (NP). 

b. Treatment of Burns: White Phosphorus (WP) and Incendiaries (TH) 
(IM) (NP). 

(3) Special medical instruction and training. 

EIGHTH HOUR—MANAGEMENT AND TRANSPORT OF CHEMICAL WARFARE 
CASUALTIES IN NAVAL AND MARINE FORCES 

a. General. 

b. Principles of. 

c. Transport of gas casualties: 

i. Afloat 
ii. Ashore 

d. Aid stations for gas contaminated casualties: 

i. Afloat 
ii. Ashore 

NINTH HOUR 

a. Resuscitation and oxygen therapy as applied to gas casualties. 

b. Contamination of food and water: 

i. General problems. 

ii. Kit, water testing and screening. 

c. Gas defense bill: Application of bill to medical organization. 

(4) Summary of course. 


a. Review. 

b. Quiz. 


TENTH HOUR 


78 


INDEX 


Paragraph 


AC (See Hydrocyanic Acid). 31 

Adamsite (See Diphenylaminechlorarsine). 17 

Ammonia . 36 

Amyl Nitrite . 31 E 

Amyl Salicylate . K)C( 6 ) ( 7 ) 

Anesthetic Solution . 10B(4) 

Anesthesia for Chemical Casualties. 5 D( 8 ) 

Apron, Impermeable . 39 E . 

Arsine (SA) . . 33 . 

Atropine Sulfate . 10B(4) 

BAL Ointment . 12 B( 2 ) 


(3) 

(4) 
12C(5) 
12E(3) 
15B(2) 


BBC (See Brombenzyl Cyanide). 16 . 

Bismuth Subcarbonate . 10 E( 2 ) 

Bismuth Subnitrate . 10 E( 2 ) 

Blister Gases . 2 A( 2 ), 9 

Blood and Nerve Poisons. 2A(5) 

30 . 

Blue Stage, Phosgene. 5B . 

Brombenzyl Cyanide (BBC) . 16 . 

Burns, Treatment of. 38 . 

Butyn Ophthalmic Ointment. 10B(4) 

Calamine Lotion N.F. 10 C( 6 ) 

Carbon Monoxide . 35 . 

Casualty Agent . 2 C( 1 ) 

CC (See Cyanogen Chloride). 32 

CG (See Phosgene). 5 

Chemical Agent Contamination of Food. 41 . 

Chemotherapy Phosgene . 5D( 6 ) 

Chemotherapy Mustard . 10B(4) (5) 

10 C( 8 )( 9 ) 
10D(3) 

Chemotherapy Burns . 38B(3) 

38C(4)(5) 

Chloracetophenone (CN) . 16 . 

Chloracetophenone Solution (CNS) 16 . 

Chloracetophenone Training Solution (CNB) . 16 . 

Chlorine . 

Chloroform, U.S.P. . 18D . 

Chlorpicrin (PS) . 6 

Pathology . 6 A 

Symptoms . 613 . 























































































Paragraph 


Page 


Diagnosis . 

Treatment . 

Prognosis . 

Choking Gases . 

Cl (See Chlorine) . 

Classification of Agents.. 

Clothing . 

CN (See Chloracetophenone). 

CNB (See Chloracetophenone Training Solution) 

CNS (See Chloracetophenone Solution). 

Contaminated Clothing . 

Contaminated Equipment . 

Contaminated Food . 

Copper Sulfate Solution. 

Cyanogen Chloride (CC). 

DA (See Diphenylchlorarsine). 

Detection of Contaminated Water. 

DC (See Diphenylcyanarsine). 

Diphosgene (DP) . 

Diphenylaminechlorarsine (DM) . 

Diphenylchlorarsine (DA) . 

Diphenylcyanarsine (DC) . 

Disinfection of Gas Masks. 

Disposition of Contaminated Clothing. 

DM (See Diphenylaminechlorarsine). 

ED (See Ethyldichlorarsine). 

Effect of Weather Conditions on Chemical Agents 

Ethyldichlorarsine (ED) . 

Expectorants, Phosgene .. 

Eye Lewisite ... 

Eye, Mustard . 

Eye, Nitrogen Mustards . 

Eye, Mixed Blister Gases... 

Eye, Lacrimators . 

Eye, Ointment BAL. 

Eluorscein . 

EM (See Titanium Tetrachloride). 

Food Contamination . 

FS (See Sulfur Trioxide-Chlorsulfonic Acid). 

Fundamentals of SELF-AID and TREATMENT 

Gas Casualty, Kit, First Aid. 

Gas Casualty Case, Treatment. 

Gas Mask, Disinfection of. 


6C . 

6 

6D . 

. 6 

6E . 

6 

2 A (T), 4 . 

. 2 

7 . 

6 

2 . 

. 2 

39 . 

. 53 

16 . 

. 33 

16 . 

. 33 

16 . 

. 33 

39 . 

. 53 

39 . 

. 53 

41 . 

. 57 

28 . 

. 39 

32 . 

. 42 

17 . 

. 35 

19 . 

. 36 

42 . 

. 61 

17 . 

. 35 

19 . 

. 36 

5 . 

. 3 

17 . 

35 

18 . 

. 35 

17 . 

35 

19 . 

. 36 

17 . 

. 35 

19 . 

. 36 

40 . 

. 55 

39C . 

. 53 

17 . 

. 35 

18 . 

. 35 

13 . 

29 

10A . 

. 10 

13 . 

29 

5D(7) . 

. 5 

12B . 

. 25 

10B . 

11 

11B 

. 20 

15B(1) . 

. 30 

16 . 

. 33 

12B(2)(3)(4) . 

. 25, 26 

10B(4) . 

12 

22 . 

37 

41 . 

. 57 

23 . 

37 

3 . 

. 2 


. 73 

. 73 

40 . 

. 55 


80 
































































































Paragraph 


Page 


Grey Stage, Phosgene. 

H (See Mustard) ... 

Harassing Agent . 

HC Mixture (HC) . 

Hydrocyanic Acid (AC). 

Hydrogen Sulfide . 

Incendiary Agents . 

Incidental Gases . 

Irritant Smokes (See vomiting Gases) 


Introduction . 

Kit, First Aid (Gas Casualty). 

Kit, Water Testing, Screening. 

L (See Lewisite) . 

Lacrimators . 

Lewisite (L) . 

General . 

Eye, Symptoms, Pathology and Prognosis. 

Eye, Decontamination of. 

Eye, procedure of decontamination with BAL 

Eye, Treatment . 

Hair, Decontamination of. 

Respiratory Tract . 

SELF-AID after Contamination. 

Skin . 

Skin, Symptoms . 

Skin, Pathology . 

Skin, Prognosis ... 

Skin, decontamination, Vapor.. 

Skin, decontamination, liquid 

Systemic . 

Treatment of Erythema. 

Treatment of Blister . 

Treatment of Denuded and Infected Burns 

Treatment of Deep Burns. 

Lung Edema . 

Lung Irritants . 

Magnesium . 

Management and Transport of Chemical Warfare 

Casualties . 

Mixed Blister Gases. 

Mustard . 

Blister . 

Erythema . 

Eye . 

Eye, decontamination of. 

Eye, Treatment of . 


5B . 


4 

10 . 


10 

2' 12) . 


2 

24 . 


38 

31 . 


41 

37 . 


46 

2C(4) . 


2 

25 . 


39 

34 . 


45 

17 . 


35 

18 . 


35 

19 . 


35 

1 . 


1 



73 

4 2D. 


62 

12 . 


25 

16 . 


33 

12 . 


25 

12A . 


25 

12 B (1) . 


25 

12B(2)(3)(4) 


25 

12B(3) . 


25 

1 2B( 5) . 


26 

12C(7) . 


28 

12D 


28 

9G. 


9 

12C . 


26 

1 2C(1) . 


26 

12C(2) . 


26 

12C(3) . 


27 

12C(4) . 


27 

12C(5) . 


27 

12E . 


28 

12C(8) . 


28 

12C(9) . 


28 

12C( 10) . 


28 

12C(11) . 


28 

5 . 


3 

4 . 


3 

27 . 


39 


43 . 69 


15 . 

. 30 

10 . 

. 10 

10C(7) . 

. 18 

10C(6) . 

. 18 

10B . 

. 11 

10B(2) . 

. 11 

10EU4) ( 5) 

11, 12 


81 
































































































Paragraph 


Page 


Gastro-Intestinal Tract . 

Hair, decontamination . 

Infected Mustard Burns, Treatment.. 

Persistence Table . 

Properties . 

Respiratory Tract . 

SELF-AID after Contamination. 

Skin . 

Skin, Decontamination of. 

Skin, Pathology . 

Skin, Symptoms . 

Skin, Treatment of. 

Systemic . 

Nitric Fumes . 

Diagnosis . 

Occurrence . 

Pathology . 

Properties . 

Prognosis . 

Symptoms . 

Treatment . 

Nitrogen Mustards (HN). 

Eyes . 

Eyes, Decontamination and Treatment 

Eyes, Symptoms and Pathology. 

Eyes, Prognosis . 

Respiration Tract . 

Gastro-Intestinal Tract . 

Skin . 

Skin, Decontamination and Treatment 

Skin, Symptoms and Pathology. 

Skin, Prognosis . 

Systemic . 

Non-Persistent Agent . 

Nose Gases (See Vomiting Gases). 


Oil Incendiaries . 

Ointment Protective 

Ointment BAL . 


Oxygen Therapy . 

PD (See Phenyldichlorarsine) 

Persistent Agent . 

Persistency Classification . 


10E . 20 

10C(5) . 17 

10C(9) . 19 

10A . 10 

10A . 10 

10D. 19 

9G. 9 

10C . 13 

10C(4) . 17 

10C(1) . 13 

I ()C (2) . 13 

10C(6) (7) (8) (9) . 18, 19 

10E . 20 

8 . 6 

8E . 7 

8B . 7 

8C . 7 

8A . 6 

8G. 7 

8D . 7 

8F . 7 

II . 20 

11B . 20 

11B(2) . 21 

11B(1) . 20 

11B(3) . 21 

1 ID. 21 

11E . 23 

11C . 21 

1 1C ( 2) . 21 

11C(1) . 21 

11C(3) . 21 

11F . 23 

2B(2) . 2 

17 . 35 

18 . 35 

19 . 36 

29 . 40 

10C(4) . 17 

15B(2) . 31 

12B(2) (3) . 25 

12C(5) . 27 

12E(3) . 29 

15B(2) . 31 

5D(3) . 4 

35G. 46 

14 . 30 

2 B ( 1) . 2 

2B . 2 


82 





























































































Persistency Table . 

Phenyldichlorarsine (PD) . 

Phosgene (CG) . 

Chemotherapy . 

Convalescent Care . 

Diagnosis . 

Expectorants . 

Pathology . 

Prognosis . 

Symptoms . 

Treatment . 

Phosphorus . 

Physiological Classification . 

Protective Ointment . 

PS (See Chlorpicrin) . 

Pulmonary Edema . 

Pulmonary Edema Treatment. 

Purification of Contaminated Water 

SA (See Arsine). 

SELF-AID, Fundamentals . 

SELF-AID . 

Screening Agents . 

Screening Smokes . 

Sedation, Phosgene . 

Sternutators (See Vomiting Gases) 


Sulfur Trioxide-Chlorsulfonic Acid (FS) 
Systemic Poisons . 

Tactical Classification . 

Tear Gases (See Lacrimators) 

TH (See Thermite) . 

Thermite (TH) . 

Titanium Tetrachloride (FM) . 

Treatment, Definitive . 

Unit No. 10 , Field Medical . 

Venesection . 

Vesicants (See Blister Gases) . 

Vomiting Gases . 

Water, Detection of Contamination 
Water, Purification of Contaminated 
Water, Testing, Screening Kit 
White Phosphorus (WP) 

WP (See White Phosphorus) . 


Paragraph Page 

10 A . 10 

14 . 30 

5 . 3 

5D(6) . 5 

. 5E . 5 

5C . 4 

• 5D(7) . 5 

. 5A. 3 

. 5F . 5 

, 5B . 4 

. 5D . 4 

.. 28 . 39 

„ 2A. 2 

10C(4) . 17 

15B(2) . 31 

.. 6 . 6 

5A. 3 

5D . 4 

42L . 66 

33 . 43 

.. 3 . 2 

.. 9G . 9 

... 2C(3) . 2 

20 . 37 

... 5D(5) . 5 

17 . 35 

18 . 35 

19 . 35 

23 . 37 

2A(5) . 2 

30 . 41 

2 C . 2 

2A(3) . 2 

16 . 33 

26 . 39 

26 . 39 

22 . 37 

3 B. 2 

.. 73 

5D(4) . 4 

2 A(2) . 2 

9 . 9 

17 . 35 

42 . 61 

42L . 66 

42D. 62 

28 . 39 

28 . 39 


☆ 590990 


83 


























































































































* ■ 

































































CHEMICAL WARFARE REFERENCE CHART 


Tactical 

Class 

Physio¬ 

logical 

Class 

Symbol 

Name 

Odor 

Color and State 

Persistence 

Effect on Body 

Protection 

Self-Aid 

Must be Immediate 



H 

Mustard 

Garlic 

Horse-radish 

Dark-oily Liquid 
Colorless Gas 

1 Day to 

All Winter 

No immediate symptoms. 

3 to 36 hours later irri¬ 
tates Eyes, Skin, Nose, 
Lungs. Worse in Tropics. 

Gas Masks 

Eye Shields 
Protective 

EYES. Wash out with water. 
SKIN. Blot off liquid. Rub in 
ointment S-461 or S-330. Do not 
use in Eyes or on reddened Skin. 
CLOTHES. See L 



HN 

Nitrogen Mustards 

Faint; Fishy 

do 

2 Hours 
to Days 


Cfl 

QJ 

c/) 

o 

L 

Lewisite 

Geraniums 

do 

1 Day to 

1 Week 

Immediate stinging pain 
of Eyes and Skin. Irri¬ 
tates Nose, Throat, and 
Lungs. Worse in Tropics. 

Clothing 

Protective 

Covers 

EYES. Squeeze ointment BAL 
into eyes. 

cn 

u 

a 

5 

ED 

Ethyldichlorarsine 

Biting and 

Stinging 

Colorless or 

Brown Liquid 
Colorless Gas 

1 to 12 

Hours 


SKIN. Blot off liquid. Rub in 
ointment BAL. Do not use on 
reddened Skin. 

CLOTHES. Remove clothing 
contaminated and discard. Avoid 
fumes. Treat underlying Skin 

w 

< 

o 

> 

H 

a 

PD 

Phenyldichlorarsine 

Shoe Polish 

Clear Viscid 

Liquid 

Hours to 
Days 



Mixed 

H and L 

HN and L, etc. 

Combination of 

H and L 

Combination of 

H and L 


Combination of 

H. and L. 


EYES. Ointment BAL. SKIN. 
Ointment S-461 or S-330. Re¬ 
move. Use BAL. CLOTHES. 
As L. 

a 

CO 

< 


CG 

Phosgene 

Musty Hay 

Green Corn 

Colorless Gas 

1 to 10 
Minutes 

Coughing. Choking. 
Difficulty in breathing. 
Fluid in Lungs. 

Gas Masks 

If breathing becomes difficult 

keep quiet and comfortably warm 
until given medical attention. 

u 

bfl 

DP 

Diphosgene 

do 

do 

30 Minutes 


Chokir 

Gases 

PS 

Chlorpicrin 

Flypaper 

Licorice 

Yellow Oily 

Liquid 

Colorless Gas 

1 Hour to 

1 Week 

Irritates Eyes. 

Same as CG. 

Gas Masks 

Rest and comfortably warm. 
Wash Eyes, Nose and Throat 
for irritation. 



CL 

Chlorine 

Chloride of 

Lime 

Greenish 

Yellow Gas 

10 Minutes 
to 1 Hour 

Same as PS. 

Gas Masks 

Same as PS. 


C/3 

~j <V c 

o-o r* o 

AC 

Hydrocyanic Acid 

Bitter Almonds 

Colorless Liquid 
or Gas 

1 to 10 
Minutes 

Dizziness, headache, 
coma. 

Gas Masks 

Whiffs of amyl nitrite. 

First aid if not breathing 
is artificial respiration. 


ocS.2 
« ££ 

CC 

Cyanogen Chloride 

Biting 

do 

do 

Irritates Eyes, Nose, 
Throat. Also as AC. 

Gas Masks 



CN 

Chloracetophenone 

Apple Blossoms 

Cloud of Particles, 
Droplets 

10 Minutes 
to Weeks 

Irritates Eyes. Heavy 
concentration irritates 

Nose, Throat, and Lungs. 
Also burns and blisters 
the skin in warm climates. 



on 

a 

Cfi 

s 

t/) 

ci 

o 

CNS 

Chloracetophenone 

Solution 

Fly Paper 

do 

1 Hour to 

1 Week 

Gas Masks 

Wash out Eyes with water and 
wash Skin with soap and water. 

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z 

cn 

u 

aJ 

QJ 

H 

CNB 

Chloracetophenone 
Training Solution 

Sweetish Benzine 

do 

Not 

determined 

Face upwind. Additional self¬ 
aid usually not necessary. 

BBC 

Brombenzyl Cyanide 

Sour Fruit 

Colorless Liquid 
or Gas 

Days to 
Weeks 



•< 

Vomiting 

Gases 

DM 

Adamsite 

Coal Smoke 

Yellow Cloud 

10 Minutes 



Sniff chloroform. Keep masked. 
Lift mask only when actually 
vomiting. Additional self-aid 

» 

X 

DA 

Diphenylchloarsine 

Shoe Polish 

White or Gray 
Cloud 

5 to 10 
Minutes 

Irritates Eyes, Nose, and 
Throat. 

Vomiting, headache. 

Gas Masks 


DC 

Diphenylcyanarsine 

Garlic 

Bitter Almonds 

White Cloud 

do 


usually not necessary. 



HC 

Hexachlorethane 

Mixture 

Sharp; Stinging 

White to Gray 
Smoke 

While 

Burning 

Heavy concentration ir¬ 
ritates Eyes, Nose, and 
Throat. 

FS and FM liquid bums 
Skin. 

Gas Masks for 
heavy concen¬ 
trations. 

Wash out Eyes if irritating. 
Wash Skin burns with water. 
Additional self-aid usually not 
necessary. 

o 

Zoo 


FS 

Sulfur Trioxide 

do 

Dense White 

Smoke 

5 to 10 
Minutes 

P 


FM 

Titanium 

do 

White Smoke 

10 Minutes 



cs § 

y(« 

c/) 


WP 

White Phosphorus 

None or 

Burning Matches 

Bums to White 
Smoke in Air 

10 Minutes 

Burns Skin. 

Avoid burning 
particles. 

Keep wet with water or cover 
with copper sulfate. Remove 
particles. Do not use grease, 
salve. 

1 


TH 

Thermite 

Magnesium Bomb 

None 

White Hot Metal; 
Bums with White 
Light 



do 

Cool burning material and re- 

INCENl 

ARIES 





Heat, burns. 


move. 

Treat as any burn. 


IM 

NP 

Thickened 

Gasoline 

Burning Oil 

Yellow Jelly 

Black Smoky 

Flame__ 


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